Talk:Smooth Muscle Development: Difference between revisions
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===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. | |||
Abstract | |||
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. | |||
PMID 22615991 | |||
==2011== | ==2011== | ||
Revision as of 10:53, 17 January 2013
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Cite this page: Hill, M.A. (2024, April 23) Embryology Smooth Muscle Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Smooth_Muscle_Development |
10 Most Recent
Note - This sub-heading shows an automated computer PubMed search using the listed sub-heading term. References appear in this list based upon the date of the actual page viewing. Therefore the list of references do not reflect any editorial selection of material based on content or relevance. In comparison, references listed on the content page and discussion page (under the publication year sub-headings) do include editorial selection based upon relevance and availability. (More? Pubmed Most Recent)
Smooth Muscle Embryology
<pubmed limit=5>Smooth Muscle Embryology</pubmed>
Smooth Muscle Development
<pubmed limit=5>Smooth Muscle Development</pubmed>
2013
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.
Abstract
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.
PMID 23319608
2012
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.
Abstract
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.
PMID 22615991
2011
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.
PMID 21677291
