Sachiko Tomita
| Faculty of Health Care and Medical Sports,Department of Medical Sports,Animal Medical Course | Professor |
Last Updated :2025/10/07
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Paper
- Diverse contribution of amniogenic somatopleural cells to cardiovascular development: With special reference to thyroid vasculature.
Yuka Haneda; Sachiko Miyagawa-Tomita; Yasunobu Uchijima; Akiyasu Iwase; Rieko Asai; Takahide Kohro; Youichiro Wada; Hiroki Kurihara
Developmental dynamics : an official publication of the American Association of Anatomists, Jan. 2024, [Reviewed]
BACKGROUND: The somatopleure serves as the primordium of the amnion, an extraembryonic membrane surrounding the embryo. Recently, we have reported that amniogenic somatopleural cells (ASCs) not only form the amnion but also migrate into the embryo and differentiate into cardiomyocytes and vascular endothelial cells. However, detailed differentiation processes and final distributions of these intra-embryonic ASCs (hereafter referred to as iASCs) remain largely unknown. RESULTS: By quail-chick chimera analysis, we here show that iASCs differentiate into various cell types including cardiomyocytes, smooth muscle cells, cardiac interstitial cells, and vascular endothelial cells. In the pharyngeal region, they distribute selectively into the thyroid gland and differentiate into vascular endothelial cells to form intra-thyroid vasculature. Explant culture experiments indicated sequential requirement of fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) signaling for endothelial differentiation of iASCs. Single-cell transcriptome analysis further revealed heterogeneity and the presence of hemangioblast-like cell population within ASCs, with a switch from FGF to VEGF receptor gene expression. CONCLUSION: The present study demonstrates novel roles of ASCss especially in heart and thyroid development. It will provide a novel clue for understanding the cardiovascular development of amniotes from embryological and evolutionary perspectives. - Coronary artery established through amniote evolution.
Kaoru Mizukami; Hiroki Higashiyama; Yuichiro Arima; Koji Ando; Norihiro Okada; Katsumi Kose; Shigehito Yamada; Jun K Takeuchi; Kazuko Koshiba-Takeuchi; Shigetomo Fukuhara; Sachiko Miyagawa-Tomita; Hiroki Kurihara
eLife, 22 Aug. 2023, [Reviewed]
Coronary arteries are a critical part of the vascular system and provide nourishment to the heart. In humans, even minor defects in coronary arteries can be lethal, emphasizing their importance for survival. However, some teleosts survive without coronary arteries, suggesting that there may have been some evolutionary changes in the morphology and function of coronary arteries in the tetrapod lineage. Here, we propose that the true ventricular coronary arteries were newly established during amniote evolution through remodeling of the ancestral coronary vasculature. In mouse (Mus musculus) and Japanese quail (Coturnix japonica) embryos, the coronary arteries unique to amniotes are established by the reconstitution of transient vascular plexuses: aortic subepicardial vessels (ASVs) in the outflow tract and the primitive coronary plexus on the ventricle. In contrast, amphibians (Hyla japonica, Lithobates catesbeianus, Xenopus laevis, and Cynops pyrrhogaster) retain the ASV-like vasculature as truncal coronary arteries throughout their lives and have no primitive coronary plexus. The anatomy and development of zebrafish (Danio rerio) and chondrichthyans suggest that their hypobranchial arteries are ASV-like structures serving as the root of the coronary vasculature throughout their lives. Thus, the ventricular coronary artery of adult amniotes is a novel structure that has acquired a new remodeling process, while the ASVs, which occur transiently during embryonic development, are remnants of the ancestral coronary vessels. This evolutionary change may be related to the modification of branchial arteries, indicating considerable morphological changes underlying the physiological transition during amniote evolution. - Cardiac neural crest lineage diversity and underlying gene regulatory networks revealed by multimodal analysis
Akiyasu Iwase; Yasunobu Uchijima; Daiki Seya; Mayuko Kida; Hiroki Higashiyama; Kazuhiro Matsui; Akashi Taguchi; Shogo Yamamoto; Shiro Fukuda; Seitaro Nomura; Takahide Kohro; Chisa Shukunami; Haruhiko Akiyama; Masahide Seki; Yutaka Suzuki; Youichiro Wada; Hiroyuki Aburatani; Yukiko Kurihara; Sachiko Miyagawa-Tomita; Hiroki Kurihara
24 Jun. 2022, [Reviewed]
Abstract
Neural crest cells (NCCs), a multipotent stem cell population, contribute to cardiac development as a source of the outflow septum, vascular smooth muscle and semilunar valves. However, genetic programs underlying lineage diversification of cardiac NCCs remain largely unknown. Using single-cell (sc) and spatial transcriptomics, we demonstrate multiple NCC subpopulations with distinct gene expression signatures; smooth muscle(-like), non-muscle mesenchymal, and Schwann cell progenitor/melanoblast-like cells. Integrative scRNA-seq and scATAC-seq analyses predict lineage trajectories starting from immature NCCs, which bifurcate into smooth muscle(-like) and non-muscle mesenchymal lineages in association with hierarchical transcription factor networks. Combinatory analyses with Cre-mediated genetic lineage tracing characterize intermediate NCCs at the bifurcation as Sox9+/Scx+ tendon and cartilage progenitor-like cells with genetic programs, some of which are common to skeletal tissues whereas others are unique to cardiac NCCs. These findings provide a basis for understanding the roles of NCCs in cardiac development and pathogenesis particularly associated with calcification. - The cardiopharyngeal mesoderm contributes to lymphatic vessel development
Kazuaki Maruyama; Sachiko Miyagawa-Tomita; Yuka Haneda; Mayuko Kida; Fumio Matsuzaki; Kyoko Imanaka-Yoshida; Hiroki Kurihara
01 Apr. 2022, [Reviewed]
ABSTRACT
Lymphatic vessels are crucial for tissue homeostasis and immune responses in vertebrates. Recent studies have demonstrated that lymphatic endothelial cells (LECs) arise from both venous sprouting (lymphangiogenesis) and de novo production from non-venous origins (lymphvasculogenesis), which is similar to blood vessel formation through angiogenesis and vasculogenesis. However, the contribution of LECs from non-venous origins to lymphatic networks is considered to be relatively small. Here, we identify the Islet1 (Isl1)-expressing cardiopharyngeal mesoderm (CPM) as a non-venous origin of craniofacial and cardiac LECs. Genetic lineage tracing with Isl1-Cre and Isl1-MerCreMer mice suggested that a subset of CPM cells gives rise to LECs. These CPM-derived LECs are distinct from venous-derived LECs in terms of their developmental processes and anatomical locations. Later, they form the craniofacial and cardiac lymphatic vascular networks in collaboration with venous-derived LECs. Collectively, our results demonstrate that there are two major sources of LECs, the cardinal vein and the CPM. As the CPM is evolutionarily conserved, these findings may improve our understanding of the evolution of lymphatic vessel development across species. Most importantly, our findings may provide clues to the pathogenesis of lymphatic malformations, which most often develop in the craniofacial and mediastinal regions. - Semaphorin3E-PlexinD1 signaling in coronary artery and lymphatic vessel development with clinical implications in myocardial recovery
Kazuaki Maruyama; Kazuaki Naemura; Yuichiro Arima; Yasunobu Uchijima; Hiroaki Nagao; Kenji Yoshihara; Manvendra K. Singh; Akiyoshi Uemura; Fumio Matsuzaki; Yutaka Yoshida; Yukiko Kurihara; Sachiko Miyagawa-Tomita; Hiroki Kurihara
iScience, Apr. 2021, [Reviewed]
Blood and lymphatic vessels surrounding the heart develop through orchestrated processes from cells of different origins. In particular, cells around the outflow tract which constitute a primordial transient vasculature, referred to as aortic subepicardial vessels, are crucial for the establishment of coronary artery stems and cardiac lymphatic vessels. Here, we revealed that the epicardium and pericardium-derived Semaphorin 3E (Sema3E) and its receptor, PlexinD1, play a role in the development of the coronary stem, as well as cardiac lymphatic vessels. In vitro analyses demonstrated that Sema3E may demarcate areas to repel PlexinD1-expressing lymphatic endothelial cells, resulting in proper coronary and lymphatic vessel formation. Furthermore, inactivation of Sema3E-PlexinD1 signaling improved the recovery of cardiac function by increasing reactive lymphangiogenesis in an adult mouse model of myocardial infarction. These findings may lead to therapeutic strategies that target Sema3E-PlexinD1 signaling in coronary artery diseases. - A temporo-spatial regulation of sema3c is essential for interaction of progenitor cells during cardiac outflow tract development
Kazuki Kodo; Shinsuke Shibata; Sachiko Miyagawa-Tomita; Sang-Ging Ong; Hiroshi Takahashi; Tsutomu Kume; Hideyuki Okano; Rumiko Matsuoka; Hiroyuki Yamagishi
Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension, 01 Jan. 2020, [Reviewed] - Amniogenic somatopleure: a novel origin of multiple cell lineages contributing to the cardiovascular system.
Rieko Asai; Yuka Haneda; Daiki Seya; Yuichiro Arima; Kimiko Fukuda; Yukiko Kurihara; Sachiko Miyagawa-Tomita; Hiroki Kurihara
Scientific reports, 21 Aug. 2017, [Reviewed]
The somatopleure is the amniotic primordium in amniote development, but its boundary to the embryonic body at early embryonic stages and the fate of cells constituting this structure are not well characterized. It also remains unclear how cells behave during the demarcation between intra- and extra-embryonic tissues. Here we identify cellular alignments, which indicate two streams towards the sites of dorsal amniotic closure and ventral thoracic wall formation. A subpopulation of mesodermal cells moving ventrally from the somatopleural region adjacent to the base of the head fold enter the body of the embryo and distribute to the thoracic wall, pharyngeal arches and heart. These cells are induced to differentiate into vascular endothelial cells and cardiomyocytes possibly by FGF and BMP signaling, respectively. These results indicate that the somatopleure acting as the amniotic primordium also serves as a source of embryonic cells, which may contribute to cardiovascular development. - Regulation of Sema3c and the Interaction between Cardiac Neural Crest and Second Heart Field during Outflow Tract Development
Kazuki Kodo; Shinsuke Shibata; Sachiko Miyagawa-Tomita; Sang-Ging Ong; Hiroshi Takahashi; Tsutomu Kume; Hideyuki Okano; Rumiko Matsuoka; Hiroyuki Yamagishi
SCIENTIFIC REPORTS, Jul. 2017, [Reviewed] - The role of the thyroid in the developing heart
Kazuhiro Maeda; Sachiko Miyagawa-Tomita; Toshio Nakanishi
Etiology and Morphogenesis of Congenital Heart Disease: From Gene Function and Cellular Interaction to Morphology, 01 Jan. 2016, [Reviewed] - Endothelin Receptor Type A-Expressing Cell Population in the Inflow Tract Contributes to Chamber Formation
Rieko Asai; Yuichiro Arima; Daiki Seya; Ki-Sung Kim; Yumiko Kawamura; Yukiko Kurihara; Sachiko Miyagawa-Tomita; Hiroki Kurihara
2016, [Reviewed]
The mammals and birds have four chambered hearts. The current models show the majority of myocardial cells derive from the first and second heart field, however, little is known regarding how heart field subpopulations contribute to specific regions in the heart. In this study, we revealed that the early Ednra-positive population in the inflow tract region contributes to the chamber myocardium by mouse-chick chimera and CreERT2/loxP lineage tracing system. - The “Cardiac Neural Crest” Concept Revisited
Sachiko Miyagawa-Tomita; Yuichiro Arima; Hiroki Kurihara
2016, [Reviewed]
Neural crest cells (NCCs) are a unique stem cell population, which originate from the border between the neural plate and surface ectoderm and migrate throughout the body to give rise to multiple cell lineages during vertebrate embryonic development. The NCCs that contribute to heart development, referred to as the cardiac NCCs, have been assigned to the neural crest at the level of the postotic hindbrain. Recently, we found that the NCCs from the preotic region migrate into the heart and partially differentiate into coronary artery smooth muscle cells. This finding indicates that the origin of the cardiac NCCs appears more widely extended to the anterior direction than Kirby et al. first designated. - Postotic and preotic cranial neural crest cells differently contribute to thyroid development
Kazuhiro Maeda; Rieko Asai; Kazuaki Maruyama; Yukiko Kurihara; Toshio Nakanishi; Hiroki Kurihara; Sachiko Miyagawa-Tomita
DEVELOPMENTAL BIOLOGY, Jan. 2016, [Reviewed] - Developmental genetic bases behind the independent origin of the tympanic membrane in mammals and diapsids
Taro Kitazawa; Masaki Takechi; Tatsuya Hirasawa; Noritaka Adachi; Nicolas Narboux-Nême; Hideaki Kume; Kazuhiro Maeda; Tamami Hirai; Sachiko Miyagawa-Tomita; Yukiko Kurihara; Jiro Hitomi; Giovanni Levi; Shigeru Kuratani; Hiroki Kurihara
Nature Communications, Nov. 2015, [Reviewed] - Distinct effects of Hoxa2 overexpression in cranial neural crest populations reveal that the mammalian hyomandibular-ceratohyal boundary maps within the styloid process.
Taro Kitazawa; Kou Fujisawa; Nicolas Narboux-Nême; Yuichiro Arima; Yumiko Kawamura; Tsuyoshi Inoue; Youichiro Wada; Takahide Kohro; Hiroyuki Aburatani; Tatsuhiko Kodama; Ki-Sung Kim; Takahiro Sato; Yasunobu Uchijima; Kazuhiro Maeda; Sachiko Miyagawa-Tomita; Maryline Minoux; Filippo M Rijli; Giovanni Levi; Yukiko Kurihara; Hiroki Kurihara
Developmental biology, 15 Jun. 2015, [Reviewed]
Most gnathostomata craniofacial structures derive from pharyngeal arches (PAs), which are colonized by cranial neural crest cells (CNCCs). The anteroposterior and dorsoventral identities of CNCCs are defined by the combinatorial expression of Hox and Dlx genes. The mechanisms associating characteristic Hox/Dlx expression patterns with the topology and morphology of PAs derivatives are only partially known; a better knowledge of these processes might lead to new concepts on the origin of taxon-specific craniofacial morphologies and of certain craniofacial malformations. Here we show that ectopic expression of Hoxa2 in Hox-negative CNCCs results in distinct phenotypes in different CNCC subpopulations. Namely, while ectopic Hoxa2 expression is sufficient for the morphological and molecular transformation of the first PA (PA1) CNCC derivatives into the second PA (PA2)-like structures, this same genetic alteration does not provoke the transformation of derivatives of other CNCC subpopulations, but severely impairs their development. Ectopic Hoxa2 expression results in the transformation of the proximal Meckel's cartilage and of the malleus, two ventral PA1 CNCCs derivatives, into a supernumerary styloid process (SP), a PA2-derived mammalian-specific skeletal structure. These results, together with experiments to inactivate and ectopically activate the Edn1-Dlx5/6 pathway, indicate a dorsoventral PA2 (hyomandibular/ceratohyal) boundary passing through the middle of the SP. The present findings suggest context-dependent function of Hoxa2 in CNCC regional specification and morphogenesis, and provide novel insights into the evolution of taxa-specific patterning of PA-derived structures. - New BRAF knockin mice provide a pathogenetic mechanism of developmental defects and a therapeutic approach in cardio-facio-cutaneous syndrome.
Shin-Ichi Inoue; Mitsuji Moriya; Yusuke Watanabe; Sachiko Miyagawa-Tomita; Tetsuya Niihori; Daiju Oba; Masao Ono; Shigeo Kure; Toshihiko Ogura; Yoichi Matsubara; Yoko Aoki
Human molecular genetics, 15 Dec. 2014, [Reviewed]
Cardio-facio-cutaneous (CFC) syndrome is one of the 'RASopathies', a group of phenotypically overlapping syndromes caused by germline mutations that encode components of the RAS-MAPK pathway. Germline mutations in BRAF cause CFC syndrome, which is characterized by heart defects, distinctive facial features and ectodermal abnormalities. To define the pathogenesis and to develop a potential therapeutic approach in CFC syndrome, we here generated new knockin mice (here Braf(Q241R/+)) expressing the Braf Q241R mutation, which corresponds to the most frequent mutation in CFC syndrome, Q257R. Braf(Q241R/+) mice manifested embryonic/neonatal lethality, showing liver necrosis, edema and craniofacial abnormalities. Histological analysis revealed multiple heart defects, including cardiomegaly, enlarged cardiac valves, ventricular noncompaction and ventricular septal defects. Braf(Q241R/+) embryos also showed massively distended jugular lymphatic sacs and subcutaneous lymphatic vessels, demonstrating lymphatic defects in RASopathy knockin mice for the first time. Prenatal treatment with a MEK inhibitor, PD0325901, rescued the embryonic lethality with amelioration of craniofacial abnormalities and edema in Braf(Q241R/+) embryos. Unexpectedly, one surviving pup was obtained after treatment with a histone 3 demethylase inhibitor, GSK-J4, or NCDM-32b. Combination treatment with PD0325901 and GSK-J4 further increased the rescue from embryonic lethality, ameliorating enlarged cardiac valves. These results suggest that our new Braf knockin mice recapitulate major features of RASopathies and that epigenetic modulation as well as the inhibition of the ERK pathway will be a potential therapeutic strategy for the treatment of CFC syndrome. - Hesr2 Knockout Mice Develop Aortic Valve Disease With Advancing Age
Hiroki Kokubo; Sachiko Miyagawa-Tomita; Yasumi Nakashima; Tsutomu Kume; Masao Yoshizumi; Toshio Nakanishi; Yumiko Saga
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Mar. 2013, [Reviewed] - Preotic neural crest cells contribute to coronary artery smooth muscle involving endothelin signalling.
Yuichiro Arima; Sachiko Miyagawa-Tomita; Kazuhiro Maeda; Rieko Asai; Daiki Seya; Maryline Minoux; Filippo M Rijli; Koichi Nishiyama; Ki-Sung Kim; Yasunobu Uchijima; Hisao Ogawa; Yukiko Kurihara; Hiroki Kurihara
Nature communications, 2012, [Reviewed]
Neural crest cells constitute a multipotent cell population that gives rise to diverse cell lineages. The neural crest arising from the postotic hindbrain is known as the 'cardiac' neural crest, and contributes to the great vessels and outflow tract endocardial cushions, but the neural crest contribution to structures within the heart remains largely controversial. Here we demonstrate that neural crest cells from the preotic region migrate into the heart and differentiate into coronary artery smooth muscle cells. Preotic neural crest cells preferentially distribute to the conotruncal region and interventricular septum. Ablation of the preotic neural crest causes abnormalities in coronary septal branch and orifice formation. Mice and chicks lacking endothelin signalling show similar abnormalities in the coronary artery, indicating its involvement in neural crest-dependent coronary artery formation. This is the first report that reveals the preotic neural crest contribution to heart development and smooth muscle heterogeneity within a coronary artery. - Effects of transforming growth factor-beta 3 and matrix metalloproteinase-3 on the pathogenesis of chronic mitral valvular disease in dogs
Koji Obayashi; Sachiko Miyagawa-Tomita; Hirotaka Matsumoto; Hidekazu Koyama; Toshio Nakanishi; Hisashi Hirose
AMERICAN JOURNAL OF VETERINARY RESEARCH, Feb. 2011, [Reviewed] - Endothelin receptor type A expression defines a distinct cardiac subdomain within the heart field and is later implicated in chamber myocardium formation
Rieko Asai; Yukiko Kurihara; Kou Fujisawa; Takahiro Sato; Yumiko Kawamura; Hiroki Kokubo; Kazuo Tonami; Koichi Nishiyama; Yasunobu Uchijima; Sachiko Miyagawa-Tomita; Hiroki Kurihara
DEVELOPMENT, Nov. 2010, [Reviewed] - An FGF autocrine loop initiated in second heart field mesoderm regulates morphogenesis at the arterial pole of the heart
Eon Joo Park; Yusuke Watanabe; Graham Smyth; Sachiko Miyagawa-Tomita; Erik Meyers; John Klingensmith; Todd Camenisch; Margaret Buckingham; Anne M. Moon
DEVELOPMENT, Nov. 2008, [Reviewed] - Activation of Notch1 signaling in cardiogenic mesoderm induces abnormal heart morphogenesis in mouse
Y Watanabe; H Kokubo; S Miyagawa-Tomita; M Endo; K Igarashi; K Aisaki; J Kanno; Y Saga
DEVELOPMENT, May 2006, [Reviewed] - Mesp1-nonexpressing cells contribute to the ventricular cardiac conduction system
S Kitajima; S Miyagawa-Tomita; T Inoue; J Kanno; Y Saga
DEVELOPMENTAL DYNAMICS, Feb. 2006, [Reviewed] - Mouse hesr1 and hesr2 genes are redundantly required to mediate Notch signaling in the developing cardiovascular system
H Kokubo; S Miyagawa-Tomita; M Nakazawa; Y Saga; RL Johnson
DEVELOPMENTAL BIOLOGY, Feb. 2005, [Reviewed] - Immunohistochemical study of apparently intact coronary artery in a child after Kawasaki disease
A Suzuki; S Miyagawa-Tomita; K Komatsu; M Nakazawa; T Fukaya; K Baba; C Yutani
PEDIATRICS INTERNATIONAL, Oct. 2004, [Reviewed] - Targeted disruption of hesr2 results in atrioventricular valve anomalies that lead to heart dysfunction
H Kokubo; S Miyagawa-Tomita; H Tomimatsu; Y Nakashima; M Nakazawa; Y Saga; RL Johnson
CIRCULATION RESEARCH, Sep. 2004 - The role of endothelin in oxygen-induced contraction of the ductus arteriosus in rabbit and rat fetuses
J Shen; T Nakanishi; H Gu; S Miyagawa-Tomita; GR Wu; K Momma; M Nakazawa
HEART AND VESSELS, Jul. 2002, [Reviewed] - ANIMAL MODELS OF VISCEROATRIAL HETEROTAXY SYNDROME IN THE RODENTS
M MORISHIMA; S MIYAGAWATOMITA; H YASUI; S MIURA; M NAKAZAWA; M ANDO; A TAKAO; K MOMMA
DEVELOPMENTAL MECHANISMS OF HEART DISEASE, 1995, [Reviewed] - MORPHOLOGICAL STUDY OF THE INV SITUS INVERSUS MUTANT MOUSE
M MORISHIMA; S MIYAGAWATOMITA; A TAKAO; M ISHIBASHI; T YOKOYAMA; PA OVERBEEK
DEVELOPMENTAL MECHANISMS OF HEART DISEASE, 1995, [Reviewed] - FUNCTIONAL CHARACTERISTICS OF THE EMBRYONIC HEART
M NAKAZAWA; M MORISHIMA; S MIYAGAWATOMITA; H TOMITA; F KAJIO
DEVELOPMENTAL MECHANISMS OF HEART DISEASE, 1995, [Reviewed] - DISTRIBUTION OF CARDIAC NEURAL CREST CELLS, FIBRONECTIN, AND TENASCIN IN THE OUTFLOW TRACT OF CHICK EMBRYOS AT INCUBATION DAY-5
S MIYAGAWATOMITA; M MORISHIMA; H TOMITA; M NAKAZAWA; K MOMMA; ML KIRBY
DEVELOPMENTAL MECHANISMS OF HEART DISEASE, 1995, [Reviewed]
MISC
- Isl1-expressing non-venous cell lineage contributes to cardiac lymphatic vessel development.
Kazuaki Maruyama; Sachiko Miyagawa-Tomita; Kaoru Mizukami; Fumio Matsuzaki; Hiroki Kurihara
Developmental biology, 15 Aug. 2019, [Reviewed]
The origin of the mammalian lymphatic vasculature has been studied for more than a century; however, details regarding organ-specific lymphatic development remain unknown. A recent study reported that cardiac lymphatic endothelial cells (LECs) stem from venous and non-venous origins in mice. Here, we identified Isl1-expressing progenitors as a potential non-venous origin of cardiac LECs. Genetic lineage tracing with Isl1-Cre reporter mice suggested a possible contribution from the Isl1-expressing pharyngeal mesoderm constituting the second heart field to lymphatic vessels around the cardiac outflow tract as well as to those in the facial skin and the lymph sac. Isl1+ lineage-specific deletion of Prox1 resulted in disrupted LYVE1+ vessel structures, indicating a Prox1-dependent mechanism in this contribution. Tracing back to earlier embryonic stages revealed the presence of VEGFR3+ and/or Prox1+ cells that overlapped with the Isl1+ pharyngeal core mesoderm. These data may provide insights into the developmental basis of heart diseases involving lymphatic vasculature and improve our understanding of organ-based lymphangiogenesis. - The Novel Contribution of Preotic Neural Crest Cells in the Coronary Artery Development
Yuichiro Arima; Sachiko Miyagawa-Tomita; Kazuhiro Maeda; Koichi Nishiyama; Rieko Asai; Yasunobu Uchijima; Hisao Ogawa; Yukiko Kurihara; Hiroki Kurihara
CIRCULATION, Nov. 2012 - A Novel Endothelin Receptor Type A-Expressing Cell Lineage Contributing to the Mouse Heart Development
Rieko Asai; Takahiro Sato; Yumiko Kawamura; Sachiko Miyagawa-Tomita; Yukiko Kurihara; Hiroki Kurihara
CIRCULATION, Oct. 2008 - Hesr, a mediator of the Notch signaling functions in heart and vessel development
H Kokubo; S Miyagawa-Tomita; RL Johnson
TRENDS IN CARDIOVASCULAR MEDICINE, Jul. 2005 - Coronary arteritis and arterial remodeling in Kawasaki disease: Immunohistochemical study
A Suzuki; S Miyagawa-Tomita; M Nakazawa; C Yutani; M Takahashi; T Otsuka; S Kawase
PEDIATRIC RESEARCH, Jan. 2003 - 冠動脈に発現する各種サイトカイン染色(共著)
2001 - 心内膜床欠損に関与する遺伝子(共著)
2001 - Staining of cytokines expressed in the human coronary artery
Organ Biology, 2001 - Molecules in atrioventricular canal defects
Gene and Medicine, 2001 - Neural crest and congenital heart diseases
Pediatrics of Japan, 2001 - Mesp1 expression is the earliest sign of cardiovascular development
Y Saga; S Kitajima; S Miyagawa-Tomita
TRENDS IN CARDIOVASCULAR MEDICINE, Nov. 2000 - Active remodeling of the coronary arterial lesions in the late phase of Kawasaki disease - Immunohistochemical study
A Suzuki; S Miyagawa-Tomita; K Komatsu; T Nishikawa; Y Sakomura; T Horie; M Nakazawa
CIRCULATION, Jun. 2000 - Remodeling of coronary artery lesions due to Kawasaki disease - Comparison of arteriographic and immunohistochemical findings
A Suzuki; S Miyagawa-Tomita; M Nakazawa; C Yutani
JAPANESE HEART JOURNAL, May 2000 - Immunohistochemical study of coronary arterial remodeling in Kawasaki disease.
A Suzuki; S Miyagawa-Tomita; M Nakazawa; K Komatsu; C Yutani
PEDIATRIC RESEARCH, Apr. 2000 - 心臓前駆細胞に発現するMesp1遺伝子(共著)
2000 - Mouse Pitx2 deficiency leads to anomalies of the ventral body wall, heart, extra- and periocular mesoderm and right pulmonary isomerism
K Kitamura; H Miura; S Miyagawa-Tomita; M Yanazawa; Y Katoh-Fukui; R Suzuki; H Ohuchi; A Suehiro; Y Motegi; Y Nakahara; S Kondo; M Yokoyama
DEVELOPMENT, Dec. 1999, [Reviewed] - MesP1 is expressed in the heart precursor cells and required for the formation of a single heart tube
Y Saga; S Miyagawa-Tomita; A Takagi; S Kitajima; J Miyazaki; T Inoue
DEVELOPMENT, Aug. 1999, [Reviewed] - Current tendency in search of molecular genes caused to congenital heart disease.Editorial comment.
1999 - Coronary vascular remodeling in Kawasaki disease:Immunohistochemical study from recovery to late phase.(共著)
1999 - Remodeling of the coronary vascular artery at late phase with Kawasaki disease.(共著)
1999 - Distribution of cardiac neural crest cells, fibronectin, and tenascin in the outflow tract of chick embryos at incubation day 5
SM Tomita; Y Tomizawa; K Waldo; ML Kirby
CIRCULATION, Oct. 1998 - Accelerated maturation of fetal ductus arteriosus by maternally administered vitamin a in rats
K Momma; M Toyono; S Miyagawa-Tomita
PEDIATRIC RESEARCH, May 1998 - Cardiac neural crest cells provide new insight into septation of the cardiac outflow tract: Aortic sac to ventricular septal closure
K Waldo; S Miyagawa-Tomita; D Kumiski; ML Kirby
DEVELOPMENTAL BIOLOGY, Apr. 1998 - Cardiac anomalies(Japanese).(共著)
1998 - Role of The Cardiac Neural Crest in Outflow Tract of Heart
MIYAGAWA-TOMITA Sachiko
Advances in animal cardiology, 1998 - 遠隔期川崎病の冠動脈リモデリングにおける免疫組織化学的検討
1998 - ウズラ-ニワトリキメラ胚の心流出路における心臓神経堤細胞:CATCH22との関係
1998 - 川崎病遠隔期の冠動脈障害リモデリングの免疫組織化学的検討-第2報-
1998 - Alterations in RAR and TGF-beta expression in developing mouse hearts exposed to retinoic acid.
#109, Scientific Conference on the genome program : Applications to cardiovascular biology. San Diego, USA, 1998 - Immunogistochermical study in progressing intimal thickening of the coronary artery with Kawasaki disease at late phase-Part II-(共著)
Prog Med, 1998 - Immunohistochemical study of progressing intimal thickening of the coronary artery at late phase in Kawasaki disease
A Suzuki; SM Tomita; M Nakazawa; K Komatsu; T Horie; Y Sakomura
CIRCULATION, Oct. 1997 - 遠隔期川崎病の冠動脈病変における増殖因子
1997 - マウス胎仔心のレチノイン酸への応答
1997 - マウス胎仔心の部域におけるレチノイン酸への応答
1997 - 川崎病冠動脈障害の遠隔期内膜肥厚の増殖因子の関連について(共著)-partI-(共著)
1997 - 小児科疾患におけるPCR(共著)
1997 - マウス胎仔の各領域におけるレチノイン酸への応答性(共著)
1997 - 川崎病冠動脈障害の遠隔期内膜肥厚における増殖因子の関与(共著)
1997 - 動脈管の胎生期発達とレチノイン酸(共著)
1997 - レチノイン酵受容体発現と発生早期のマウス胎仔心の領域特異性(共著)
1997 - Expression of TGF beta genes is regionally specific in mouse embryonic hearts.
1997 - Alterations in TGF beta and RAR expression in developing mouse hearts exposed to retinoic acid.
Weinstein Cardiovasc Dev Conf, IV-15, Philadelphia, USA, 1997 - Immunohistochemical study in progresing intimal thickening of the coronary artery with kawasaki disease at late phase-Part 1-
Progress in Medicine, 1997 - PCR in Pediatrio disease
1997 - Pathological study of Japanese quail embryo with acid alpha-glucosidase deficiency during early development
S MiyagawaTomita; M Morishima; M Nakazawa; M Mizutani; T Kikuchi
ACTA NEUROPATHOLOGICA, Sep. 1996 - MORPHOLOGICAL OBSERVATIONS ON THE PATHOGENETIC PROCESS OF TRANSPOSITION OF THE GREAT-ARTERIES INDUCED BY RETINOIC ACID IN MICE
H YASUI; M NAKAZAWA; M MORISHIMA; S MIYAGAWATOMITA; K MOMMA
CIRCULATION, May 1995 - 心臓の形態発生とその異常
1995 - Visceroatrial heterotaxy syndrome induced by maternal hyperthermia in the rat
Masae Morishima; Sachiko Miyagawa-Tomita; Hiroshi Yasui; Masahiko Ando; Makoto Nakazawa; Atsuyoshi Takao
Cardiology in the Young, 1995 - HEMODYNAMICS AND VENTRICULAR-FUNCTION IN THE DAY-12 RAT EMBRYO - BASIC CHARACTERISTICS AND THE RESPONSES TO CARDIOVASCULAR DRUGS
M NAKAZAWA; M MORISHIMA; H TOMITA; SM TOMITA; F KAJIO
PEDIATRIC RESEARCH, Jan. 1995 - Cardiac morphology and the anomalies.
Associate Doctors and Students, 1995 - Expression of RARs and TGF-β1 genes in developmental mouse embpryonic hearts(共著)
X1th Scientfic Sessions of International Society for heart research Japanese section, 1994 - レチノイン酸によって誘発された、完全大血管転換症マウス胚の心ループの形態学的観察
1993 - ニワトリ5日胚の心流出路における心臓神経堤細胞とファイブロネクチン、テネイシンの分布
1993 - ウズラ、ニワトリキメラにおける心臓神経堤細胞の移動と分布(共著)
1993 - レチノイン酸投与マウスにおける大血管転換症(TGA)の形態学的特徴(共著)
1993 - Distribution of cardiac neural crest cells, fibronectin and tenastin in the outflow of chick empbryts at incubation day 5.(共著)
4th Int Sympoen Etiology and Morphogenesis of Heart Disease 7, 1993 - RETINOIC ACID AMBIVALENTLY REGULATES THE EXPRESSION OF MYOD1 IN THE MYOGENIC CELLS IN THE LIMB BUDS OF THE EARLY DEVELOPMENTAL STAGES
T MOMOI; S MIYAGAWATOMITA; S NAKAMURA; KIMURA, I; M MOMOI
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Aug. 1992 - CELLULAR RETINOIC ACID BINDING-PROTEIN TYPE-II WAS PREFERENTIALLY LOCALIZED IN MEDIUM AND POSTERIOR PARTS OF THE PROGRESS ZONE OF THE CHICK LIMB BUD
S MIYAGAWATOMITA; T KITAMOTO; K MOMMA; A TAKAO; T MOMOI
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, May 1992 - Molecular mechanism of neurogenesis and retinoic acid(Japanese).(共著)
1992 - 神経発生分化の分子メカニズムとレチノイン酸(共著)
1992 - 形態形成とレチノイン酸レセプターの分布(共著)
1992 - Molecular mechenism of neurgenesis and retinoic acid.
Biomedica, 1992 - Morphclayy and the distnhition of retinoic and vceptor.
Hdebolosm and disease, 1992 - Effect of atrial natriuretic peptide of cardiovascular function in the rat embryo. (共著)
Acta Cardiol Paediatr Japonica, 1992 - EFFECTS OF ENVIRONMENTAL HYPERTHERMIA ON CARDIOVASCULAR FUNCTION IN THE RAT EMBRYO
M NAKAZAWA; ST MIYAGAWA; M MORISHIMA; F KAJIO; A TAKAO
PEDIATRIC RESEARCH, Dec. 1991 - TEMPOROSPATIAL STUDY OF THE MIGRATION AND DISTRIBUTION OF CARDIAC NEURAL CREST IN QUAIL-CHICK CHIMERAS
S MIYAGAWATOMITA; K WALDO; H TOMITA; ML KIRBY
AMERICAN JOURNAL OF ANATOMY, Sep. 1991 - FETAL CARDIOVASCULAR MORPHOLOGY OF TRUNCUS ARTERIOSUS WITH OR WITHOUT TRUNCAL VALVE INSUFFICIENCY IN THE RAT
K MOMMA; M ANDO; A TAKAO; S MIYAGAWATOMITA
CIRCULATION, Jun. 1991 - SEGMENTAL EXPRESSION OF CELLULAR RETINOIC ACID BINDING-PROTEIN (TYPE-I) IN RHOMBOMERES OF THE EARLY CHICK-EMBRYO
S MIYAGAWATOMITA; K KOMATSU; K MOMMA; M MOMOI; T MOMOI
BIOMEDICAL RESEARCH-TOKYO, Jun. 1991 - DEVELOPMENT OF CRANIAL NERVES IN THE CHICK-EMBRYO WITH SPECIAL REFERENCE TO THE ALTERATIONS OF CARDIAC BRANCHES AFTER ABLATION OF THE CARDIAC NEURAL CREST
SC KURATANI; S MIYAGAWATOMITA; ML KIRBY
ANATOMY AND EMBRYOLOGY, 1991 - THE EFFECTS OF HIGH PHENYLALANINE CONCENTRATION ON CHICK EMBRYONIC-DEVELOPMENT
ML KIRBY; ST MIYAGAWA
JOURNAL OF INHERITED METABOLIC DISEASE, 1990 - THE EXPRESSION OF RETINOIC ACID RECEPTOR IN THE CHICK LIMB BUD DURING EARLY DEVELOPMENTAL STAGES
T MOMOI; M MOMOI; H KUMAGAI; H UTSUMI; S MIYAGAWATOMITA; A TAKAO
PROCEEDINGS OF THE JAPAN ACADEMY SERIES B-PHYSICAL AND BIOLOGICAL SCIENCES, Oct. 1989 - HEMODYNAMIC-EFFECTS OF ACETYLCHOLINE IN THE CHICK-EMBRYO AND DIFFERENCES FROM THOSE IN THE RAT EMBRYO
M NAKAZAWA; T OHNO; S MIYAGAWA; A TAKAO
TERATOLOGY, Jun. 1989 - EFFECT OF ENVIRONMENTAL HYPERTHERMIA ON HEMODYNAMICS OF THE 12 DAY RAT EMBRYO
M NAKAZAWA; S MIYAGAWA; A TAKAO
PEDIATRIC RESEARCH, Apr. 1989 - PATHOGENESIS OF PERSISTENT TRUNCUS ARTERIOSUS INDUCED BY NIMUSTINE HYDROCHLORIDE IN CHICK-EMBRYOS
S MIYAGAWA; ML KIRBY
TERATOLOGY, Mar. 1989 - CARDIOVASCULAR ANOMALIES PRODUCED BY NIMUSTINE HYDROCHLORIDE IN THE RAT FETUS
S MIYAGAWA; M ANDO; A TAKAO
TERATOLOGY, Dec. 1988 - RETINOIC ACID-INDUCED HETEROTAXY SYNDROME IN RAT EMBRYOS
S MIURA; S MIYAGAWA; M ANDO; A TAKAO
TERATOLOGY, Nov. 1988 - HEART-RATE AND BLOOD-PRESSURE, AND THEIR RESPONSE TO ACETYLCHOLINE IN NEURAL CREST CELL EXCISED CHICK-EMBRYOS
M NAKAZAWA; S MIYAGAWA; M NISHIBATAKE; A TAKAO
TERATOLOGY, Nov. 1988 - Hemodynamic characteristics in neural crest cell-excised chick embryo
Makoto Nakazawa; Sachiko Miyagawa; Makoto Nishibatake; Kazuo Ikeda; Atsuyoshi Takao
Heart and Vessels, Sep. 1988
Springer-Verlag - DEVELOPMENTAL HEMODYNAMIC-CHANGES IN RAT EMBRYOS AT 11 TO 15 DAYS OF GESTATION - NORMAL DATA OF BLOOD-PRESSURE AND THE EFFECT OF CAFFEINE COMPARED TO DATA FROM CHICK-EMBRYO
M NAKAZAWA; S MIYAGAWA; T OHNO; S MIURA; A TAKAO
PEDIATRIC RESEARCH, Feb. 1988 - Hemodynamic effects of acetylcholine in chick embryos(Japanese).(共著)
1988 - DIFFERENCE IN HEMODYNAMIC-RESPONSE TO CAFFEINE BETWEEN THE CHICK AND RAT EMBRYOS
M NAKAZAWA; S MIYAGAWA; A TAKAO
TERATOLOGY, Dec. 1987 - MICROANGIOGRAPHIC ANALYSIS OF BLOOD-FLOW PATTERN DURING EARLY CARDIOVASCULAR MORPHOGENESIS IN THE CHICK-EMBRYO
M NISHIBATAKE; M NAKAZAWA; S MIYAGAWA; ML KIRBY
CIRCULATION, Oct. 1987 - Effect of bisdiamine on a rat embryo: A hemodynamic study(Japanese).(共著)
1987 - BLOOD-PRESSURE MEASUREMENT IN THE RAT EMBRYO FROM 11 TO 15 GESTATIONAL DAYS
M NAKAZAWA; S MIYAGAWA; A TAKAO
TERATOLOGY, Dec. 1986 - TERATOGENIC EFFECT OF RETINOIC ACID ON RAT FETUSES
S MIURA; S MIYAGAWA; M ANDO; A TAKAO
TERATOLOGY, Dec. 1986 - HEMODYNAMIC-EFFECTS OF ENVIRONMENTAL HYPERTHERMIA IN STAGE-18, STAGE-21, AND STAGE-24 CHICK-EMBRYOS
M NAKAZAWA; S MIYAGAWA; A TAKAO; EB CLARK; N HU
PEDIATRIC RESEARCH, Dec. 1986 - DEVELOPMENTAL HEMODYNAMIC-CHANGES IN THE RAT EMBRYO FROM 11 TO 15 GESTATIONAL DAYS
M NAKAZAWA; S MIYAGAWA; A TAKAO
CIRCULATION, Oct. 1986 - CONTRIBUTION OF NEURAL CREST CELLS TO CARDIOGENESIS - MICROSURGERY OF CRANIAL NEURAL CREST IN CHICK-EMBRYOS
S MIYAGAWA; M ANDO; A TAKAO
JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION, Aug. 1986 - Developmental hemodynamic changes in the rat embryo from 11 to 15 gestational days(Japanese).(共著)
1986 - Cardiovascular effects of isoproterenol in the stage 21 chick embryo(Japanese).(共著)
1986 - CARDIOVASCULAR ANOMALIES INDUCED IN FETAL RATS BY NIMUSTINE HYDROCHLORIDE
S MIYAGAWA; M ANDO; A TAKAO
TERATOLOGY, 1985 - Human congenital heart disease-conotruncus anomaly(Japanese).(共著)
1985 - Incomplete atrioventricular canal malformation with subaortic stenosis in a pig(Japanese).(共著)
1984 - Transvenous left heart contrast echocardiography: A technical evaluation and a consideration of its mechanisms(Japanese).(共著)
1983 - Feline heart diseases(Japanese).(共著)
1982 - Subvalvular Aortic Stenosis with Ventricular Septal Defect in a Cat
MIYAGAWA Sachiko; HASEGAWA Atsuhiko; HIROSE Hisashi; GOTO Naoaki; KOGURE Kazuo; ANDO Masahiko
Advances in Animal Cardiology, 1981
Clinical and pathological findings of subvalvular aortic stensosis with ventricular septal defect (VSD) in a one-year-old female domestic short-haired cat were described.
The cat revealed laboured breathing, tachycardia, hepatomegaly, and ascites. A systolic murmur was heard on both sides of the chest. The chest x-ray demonstrated severe cardiomegaly (CTR:80%) and pleural effusion. Electrocardiogram and vectorcardiogram showed combined ventricular hypertrophy with a dominant right ventricular force and biatrial hypertrophy.
Subvalvular aortic stenosis was present about 2 mm below the aortic valve and immediately above the VSD. The obstruction of about 2 mm opening in the sub-aortic area was formed by a fibrous membrane and the anterior leaflet of the mitral valve adhered to the ventricular septum., Japanese Society of Veterinary Cardiology - Vectorcardiogram of the normal cat recorded by the heartorthogonal lead system(Japanese).(共著)
1979 - A case of canine cryptococcosis(Japanese).(共著)
1978 - Difference in form of sialic acid in red blood cell glycolipids of different breeds of dogs.(共著)
J Biochem, 1978
Books and other publications
- Endothelin receptor type A-expressing cell population in the inflow tract contributes to chamber formation. (共著）
Asai R
Etiology and morphogenesis of congenital heart disease. . Springer, 2016 - The role of the thyroid in the developing heart（共著）
Maeda K
Etiology and morphogenesis of congenital heart disease. Springer, 2016 - The “cardiac neural crest” concept revisited (共著）
MIYAGAWA-TOMITA Sachiko
Etiology and morphogenesis of congenital heart disease. Springer, 2016 - 心臓形態形成とその異常。
1999 - Cardiogenesis and the anomalies.
Veterinary Medical Care Handbook-The Latest Review-.Interzoo,Tokyo,Japan, 1999 - レチノイン酸と発達心 臨床発達心臓病学、第2版(共著)
1997 - 刺激伝導系の発達 臨床発達心臓病学、第2版(共著)
1997 - 心臓の発生と発達を制御する分子経路(共著) 臨床発達心臓病学、第2版
1997 - 岩波生物学辞典第4版(共著)
1996 - 心奇形発生のメカニズムは(共著)
1995 - Functional characteristics of the embryonic heart.(共著)
Developmental Mechanisms of Heart Disease.Futura,New York, 1995 - Functional characteristics of the embryonic heart. Developmental Mechanisms of Heart Disease.
Fututa, New York, 1995 - Animal models of visceroatrial heterotaxy syndrome in the rodents. (共著)Developmental Mechanisms of Heart Disease.
Futura, New York, 1995 - Morphological study of the inv situs inversus mutant mouse. (共著)Developmental MEchanisms of Heart Disease.
Futura, New York, 1995 - Mechanison of the developmental congenital heart anomalies
1995 - Distribution of cardiac neural crest cells, dibronection and tenascin in the outflow tract of chick embryos at incubation day 5 (共著)
Developmental Mechanisms of Heart Disease Futura,New York, 1995 - Effect of bisdiamine given to pregnant rats on hemodynamics of their embryos.(共著)
Embryonic origins of defective heart development.Annals of the New York Academy of Sciences, 1990 - Retinoic acid-induced visceroatrical heterotaxy syndrome in rat fetus.(共著)
Developmental cardiology:Morphogenesis and function.Futura,New York, 1990 - Migration of cardiac neural crest cells a temporo to spatial study in early quail-chick chimeras (共著)
Embryonic origins of defective heart development. Annals of the New York Academy of Sciences, 1990 - Hemodynamic effects of cardiovascular agents on the embryonic circulation : a comparative study in chick and rat embryos.(共著)
Developmental cardiology:Morphogenesis and function.Futura,New York, 1989 - AV canal defect in a feline species.(共著)
Congenital Heart Disease.Futura,New York, 1984
Works
- jumonji遺伝子の心臓発生での機能と心筋再生
2000 - 2001 - 心臓房室心内膜床欠損の形態におけるPitx2遺伝子の機能
2000 - 2001 - Roles of jumonji gene in cardiac development and regeneration
2000 - 2001 - Pitx2 function in morphogenesis of atrioventricular septal defect
2000 - 2001 - Mesp転写因子による心臓前駆細胞の分化
2001 - Differentiation of cardiac progenitor cells in Me transcription factor
2001
Research Themes
- Cooperation of neural crest cells, macrophages, and vascular endothelial cells during cardiac development.
Grant-in-Aid for Scientific Research (C)
Yamazaki University of Animal Nursing
01 Apr. 2022 - 31 Mar. 2025 - 縦隔間葉系の器官発生及び疾患発症における意義の解明
09 Jul. 2021 - 31 Mar. 2024 - Comprehensive research in morphogenesis of the cardiac outflow tract
Grant-in-Aid for Scientific Research (C)
Yamazaki University of Animal Nursing
01 Apr. 2019 - 31 Mar. 2022
The cardiac outflow tract is the region that connects the myocardium to the blood vessels, and abnormalities in this region are most frequent in congenital heart disease. The cells forming the cardiac outflow tract include second heart field derived cells, cardiac neural crest cells(postotic nccs), preotic nccs, intra-embryonic amniogenic somatopleural mesodermal cells, and epicardial progenitor cells. The purpose of this study is to construct a system to capture the morphogenetic process of the cardiac outflow tract during development in three dimensions and to elucidate the entire picture. We confirmed the distribution of nccs in the aortic and pulmonary valves in the neural crest marker Wnt-1-Cre mice. Furthermore, we found that the distribution of preotic and postotic nccs in the aortic and pulmonary valves differed in the chick chimara embryos. - Integrative understanding of the development, evolution, disease and regeneration of the coronary circulatory system based on multicellular interaction
Grant-in-Aid for Scientific Research (A)
The University of Tokyo
01 Apr. 2019 - 31 Mar. 2022
We have revealed that the coronary artery origin is formed through a multi-cellular interaction involving various cell types, including the secondary heart field-derived endothelial cells and neural crest-derived smooth muscle cells, as well as epicardial cells and macrophages, via signals such as endothelin and Sema3E-PlexinD1, during coronary circulation development. In addition, comparative developmental anatomy of vertebrate coronary arteries suggests that the origin of coronary arteries in mammals may be an evolutionary novelty. Furthermore, experiments using a mouse myocardial infarction model revealed that inactivation of Sema3E-PlexinD1 signaling improved the recovery of cardiac function by increasing reactive lymphangiogenesis, leading to therapeutic strategies that target Sema3E-PlexinD1 signaling in coronary artery diseases. - Exploring the mechanism of cardiac development and regeneration based on diverse cellular origins
Grant-in-Aid for Scientific Research (A)
The University of Tokyo
01 Apr. 2015 - 31 Mar. 2018
We identified the preotic neural crest and amniogenic somatopleural mesoderm as novel origins of cardiovascular components, found phenotypic diversity within each lineage by single-cell transcriptome analysis, and revealed signals that possibly regulate their differentiation and migration. In coronary artery development, we found the involvement of coordination between cells giving rise to the coronary ostia and forming lymphatic vessels. The signaling molecules mediating their interaction are also involved in post-ischemic cardiac injury, which indicates their potential as a novel therapeutic target in myocardial infarction. - Characterization of neural crest cells migrating into the heart
Grant-in-Aid for Challenging Exploratory Research
The University of Tokyo
01 Apr. 2014 - 31 Mar. 2016
In this study, we investigated the origin and fate of neural crest cells migrating into the heart through experiments using mouse and avian embryos. We found that cells originating from the preotic region of the neural crest, as well as “cardiac neural crest cells” derived from the more caudal post-otic region, migrate into the heart and differentiate into various cell types including coronary artery smooth muscle cells and mesenchymal cells in the semiluminal valves and myocardial walls. Single-cell analysis of gene expression patterns revealed the existence of a subset of neural crest cells expressing some stem cell markers (e.g. c-Kit), indicating the maintenance of the stemness with multipotency in a neural crest population within the heart. - Establishment of the concept of broad organ-forming network in cardiovascular formation and models for tissue reconstruction
Grant-in-Aid for Scientific Research (A)
The University of Tokyo
01 Apr. 2012 - 31 Mar. 2016
In this study, we identified the preotic cranial neural crest, which gives rise to craniofacial skeletons especially in the pharyngeal arch-derived structures, as a novel origin of cells constituting the heart to differentiate into coronary artery smooth muscle cells and other various cell types. In addition, we discovered another novel candidate origin of the heart in a region of mesoderm, which may contribute to cardiomyocytes and vascular endothelial cells. These cells from novel origins may participate in cardiovascular differentiation and morphogenesis through cell-to-cell interactions via signaling molecules such as endothelin and semaphorin-plexin. Identification of these cell origins and lineages enables us to analyze a broad cellular network to drive organogenesis and to establish different models for tissue regeneration from a novel viewpoint. - Role of neural crest cells in bicuspic aortic valve
Grant-in-Aid for Scientific Research (C)
Apr. 2013 - Mar. 2016 - Identification of novel cell lineages contributing to cardiovascular development and clarification of mechanisms underlying their fate determination
Grant-in-Aid for Scientific Research (B)
The University of Tokyo
2009 - 2011
Early endothelin receptor type A expression defines a subdomain of the first heart field contributing to chamber formation, in which endothelin signaling is involved by stimulating ERK phosphorylation and Tbx5 expression. In angiogenesis, complex cell behavior and tip cell overtaking were revealed to contribute to branching morphogenesis by a time-lapse imaging and computer-assisted analysis. - Analysis of Pitx2 function in formation of the AV cushions of heart
- Growth factor in the coronary antery with kawasaki disease
- Molecular study in cardiac vascular system at developmental embryo
