Talk:Smooth Muscle Development
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Cite this page: Hill, M.A. (2019, September 17) Embryology Smooth Muscle Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Smooth_Muscle_Development
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Smooth Muscle Embryology
<pubmed limit=5>Smooth Muscle Embryology</pubmed>
Smooth Muscle Development
<pubmed limit=5>Smooth Muscle Development</pubmed>
Heterogeneity in vascular smooth muscle cell embryonic origin in relation to adult structure, physiology, and disease
Dev Dyn. 2015 Mar;244(3):410-6. doi: 10.1002/dvdy.24247.
Pfaltzgraff ER, Bader DM.
Regional differences in vascular physiology and disease response exist throughout the vascular tree. While these differences in physiology and disease correspond to regional vascular environmental conditions, there is also compelling evidence that the embryonic origins of the smooth muscle inherent to the vessels may play a role. Here, we review what is known regarding the role of embryonic origin of vascular smooth muscle cells during vascular development. The focus of this review is to highlight the heterogeneity in the origins of vascular smooth muscle cells and the resulting regional physiologies of the vessels. Our goal is to stimulate future investigation into this area and provide a better understanding of vascular organogenesis and disease. . © 2014 Wiley Periodicals, Inc. KEYWORDS: cellular origins and fates; embryonic development; vascular organogenesis PMID 25546231
Embryonic origins of human vascular smooth muscle cells: implications for in vitro modeling and clinical application
Cell Mol Life Sci. 2014 Jun;71(12):2271-88. doi: 10.1007/s00018-013-1554-3. Epub 2014 Jan 18.
Sinha S1, Iyer D, Granata A.
Vascular smooth muscle cells (SMCs) arise from multiple origins during development, raising the possibility that differences in embryological origins between SMCs could contribute to site-specific localization of vascular diseases. In this review, we first examine the developmental pathways and embryological origins of vascular SMCs and then discuss in vitro strategies for deriving SMCs from human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). We then review in detail the potential for vascular disease modeling using iPSC-derived SMCs and consider the pathological implications of heterogeneous embryonic origins. Finally, we touch upon the role of human ESC-derived SMCs in therapeutic revascularization and the challenges remaining before regenerative medicine using ESC- or iPSC-derived cells comes of age.
Prdm6 is essential for cardiovascular development in vivo
PLoS One. 2013 Nov 21;8(11):e81833. doi: 10.1371/journal.pone.0081833.
Gewies A, Castineiras-Vilarino M, Ferch U, Jährling N, Heinrich K, Hoeckendorf U, Przemeck GK, Munding M, Groß O, Schroeder T, Horsch M, Karran EL, Majid A, Antonowicz S, Beckers J, Hrabé de Angelis M, Dodt HU, Peschel C, Förster I, Dyer MJ, Ruland J. Source Institut für Klinische Chemie und Pathobiochemie, Klinikum Rechts der Isar, Technische Universität München, Munich, Germany ; German Cancer Consortium (DKTK), Heidelberg, Germany ; German Cancer Research Center (DKFZ), Heidelberg, Germany ; Laboratory of Signaling in the Immune System, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany.
Members of the PRDM protein family have been shown to play important roles during embryonic development. Previous in vitro and in situ analyses indicated a function of Prdm6 in cells of the vascular system. To reveal physiological functions of Prdm6, we generated conditional Prdm6-deficient mice. Complete deletion of Prdm6 results in embryonic lethality due to cardiovascular defects associated with aberrations in vascular patterning. However, smooth muscle cells could be regularly differentiated from Prdm6-deficient embryonic stem cells and vascular smooth muscle cells were present and proliferated normally in Prdm6-deficient embryos. Conditional deletion of Prdm6 in the smooth muscle cell lineage using a SM22-Cre driver line resulted in perinatal lethality due to hemorrhage in the lungs. We thus identified Prdm6 as a factor that is essential for the physiological control of cardiovascular development.
Brg1 governs distinct pathways to direct multiple aspects of mammalian neural crest cell development
Proc Natl Acad Sci U S A. 2013 Jan 14. [Epub ahead of print]
Li W, Xiong Y, Shang C, Twu KY, Hang CT, Yang J, Han P, Lin CY, Lin CJ, Tsai FC, Stankunas K, Meyer T, Bernstein D, Pan M, Chang CP. Source Division of Cardiovascular Medicine, Department of Medicine, Department of Chemical and Systems Biology, and Division of Pediatric Cardiology, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305.
Development of the cerebral vessels, pharyngeal arch arteries (PAAs). and cardiac outflow tract (OFT) requires multipotent neural crest cells (NCCs) that migrate from the neural tube to target tissue destinations. Little is known about how mammalian NCC development is orchestrated by gene programming at the chromatin level, however. Here we show that Brahma-related gene 1 (Brg1), an ATPase subunit of the Brg1/Brahma-associated factor (BAF) chromatin-remodeling complex, is required in NCCs to direct cardiovascular development. Mouse embryos lacking Brg1 in NCCs display immature cerebral vessels, aberrant PAA patterning, and shortened OFT. Brg1 suppresses an apoptosis factor, Apoptosis signal-regulating kinase 1 (Ask1), and a cell cycle inhibitor, p21(cip1), to inhibit apoptosis and promote proliferation of NCCs, thereby maintaining a multipotent cell reservoir at the neural crest. Brg1 also supports Myosin heavy chain 11 (Myh11) expression to allow NCCs to develop into mature vascular smooth muscle cells of cerebral vessels. Within NCCs, Brg1 partners with chromatin remodeler Chromodomain-helicase-DNA-binding protein 7 (Chd7) on the PlexinA2 promoter to activate PlexinA2, which encodes a receptor for semaphorin to guide NCCs into the OFT. Our findings reveal an important role for Brg1 and its downstream pathways in the survival, differentiation, and migration of the multipotent NCCs critical for mammalian cardiovascular development.
Notch2 and Notch3 function together to regulate vascular smooth muscle development
PLoS One. 2012;7(5):e37365. doi: 10.1371/journal.pone.0037365. Epub 2012 May 17.
Wang Q, Zhao N, Kennard S, Lilly B. Source Center for Cardiovascular and Pulmonary Research, Nationwide Children's Hospital, Columbus, Ohio, United States of America.
Notch signaling has been implicated in the regulation of smooth muscle differentiation, but the precise role of Notch receptors is ill defined. Although Notch3 receptor expression is high in smooth muscle, Notch3 mutant mice are viable and display only mild defects in vascular patterning and smooth muscle differentiation. Notch2 is also expressed in smooth muscle and Notch2 mutant mice show cardiovascular abnormalities indicative of smooth muscle defects. Together, these findings infer that Notch2 and Notch3 act together to govern vascular development and smooth muscle differentiation. To address this hypothesis, we characterized the phenotype of mice with a combined deficiency in Notch2 and Notch3. Our results show that when Notch2 and Notch3 genes are simultaneously disrupted, mice die in utero at mid-gestation due to severe vascular abnormalities. Assembly of the vascular network occurs normally as assessed by Pecam1 expression, however smooth muscle cells surrounding the vessels are grossly deficient leading to vascular collapse. In vitro analysis show that both Notch2 and Notch3 robustly activate smooth muscle differentiation genes, and Notch3, but not Notch2 is a target of Notch signaling. These data highlight the combined actions of the Notch receptors in the regulation of vascular development, and suggest that while these receptors exhibit compensatory roles in smooth muscle, their functions are not entirely overlapping.
Smooth muscle cell differentiation in vitro: models and underlying molecular mechanisms
Arterioscler Thromb Vasc Biol. 2011 Jul;31(7):1485-94.
Xie C, Ritchie RP, Huang H, Zhang J, Chen YE. Source Cardiovascular Center, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI, USA. Abstract Development of in vitro models by which to study smooth muscle cell (SMC) differentiation has been hindered by some peculiarities intrinsic to these cells, namely their different embryological origins and their ability to undergo phenotypic modulation in cell culture. Although many in vitro models are available for studying SMC differentiation, careful consideration should be taken so that the model chosen fits the questions being posed. In this review, we summarize several well-established in vitro models available to study SMC differentiation from stem cells and outline novel mechanisms recently identified as underlying SMC differentiation programs.