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Smooth muscle myosin heavy chain exclusively marks the smooth muscle lineage during mouse embryogenesis.

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TLDR
Results indicate that smooth muscle myogenesis begins by 10.5 days of embryonic development in the mouse and establish SM-MHC as a highly specific marker for the SMC lineage.
Abstract
We cloned a portion of the mouse smooth muscle myosin heavy chain (SM-MHC) cDNA and analyzed its mRNA expression in adult tissues, several cell lines, and developing mouse embryos to determine the suitability of the SM-MHC promoter as a tool for identifying smooth muscle-specific transcription factors and to define the spatial and temporal pattern of smooth muscle differentiation during mouse development. RNase protection assays showed SM-MHC mRNA in adult aorta, intestine, lung, stomach, and uterus, with little or no signal in brain, heart, kidney, liver, skeletal muscle, spleen, and testes. From an analysis of 14 different cell lines, including endothelial cells, fibroblasts, and rhabdomyosarcomas, we failed to detect any SM-MHC mRNA; all of the cell lines induced to differentiate also showed no detectable SM-MHC. In situ hybridization of staged mouse embryos first revealed SM-MHC transcripts in the early developing aorta at 10.5 days post coitum (dpc). No hybridization signal was demonstrated beyond the aorta and its arches until 12.5 to 13.5 dpc, when SM-MHC mRNA appeared in smooth muscle cells (SMCs) of the developing gut and lungs as well as peripheral blood vessels. By 17.5 dpc, SM-MHC transcripts had accumulated in esophagus, bladder, and ureters. Except for blood vessels, no SM-MHC transcripts were ever observed in developing brain, heart, or skeletal muscle. These results indicate that smooth muscle myogenesis begins by 10.5 days of embryonic development in the mouse and establish SM-MHC as a highly specific marker for the SMC lineage. The SM-MHC promoter should therefore serve as a useful model for defining the mechanisms that govern SMC transcription during development and disease.

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Molecular Regulation of Vascular Smooth Muscle Cell Differentiation in Development and Disease

TL;DR: The focus of this review is to provide an overview of the current state of knowledge of molecular mechanisms/processes that control differentiation of vascular smooth muscle cells (SMC) during normal development and maturation of the vasculature, as well as how these mechanisms/ processeses are altered in vascular injury or disease.
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Vascular Extracellular Matrix and Arterial Mechanics

TL;DR: By correlating vessel mechanics with physiological blood pressure across animal species and in mice with altered vessel compliance, it is shown that cardiac and vascular development are physiologically coupled, and there is evidence for a universal elastic modulus that controls the parameters of ECM deposition in vessel wall development.
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PDGF, TGF-β, and Heterotypic Cell–Cell Interactions Mediate Endothelial Cell–induced Recruitment of 10T1/2 Cells and Their Differentiation to a Smooth Muscle Fate

TL;DR: In vitro and in vivo observations shed light on the cell–cell interactions that occur during vessel development, as well as in pathologies in which developmental processes are recapitulated.
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Regulation and characteristics of vascular smooth muscle cell phenotypic diversity

TL;DR: This review discusses recent literature demonstrating the extent and nature of smooth muscle cell diversity in the vascular wall and addresses the factors that affect smoother muscle cell phenotype.
References
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Journal ArticleDOI

Single-step method of RNA isolation by acid guanidinium thiocyanate-phenol-chloroform extraction

TL;DR: A new method of total RNA isolation by a single extraction with an acid guanidinium thiocyanate-phenol-chloroform mixture is described, providing a pure preparation of undegraded RNA in high yield and can be completed within 4 h.
Journal ArticleDOI

Neural Crest Cells Contribute to Normal Aorticopulmonary Septation

TL;DR: By analyzing the hearts of quail-chick chimeras, it was found that neural crest cells at the level of occipital somites 1 to 3 migrate to the region of the aorticopulmonary septum, resulting in common arterial outflow channels or transposition of the great vessels.
Journal ArticleDOI

The gene tinman is required for specification of the heart and visceral muscles in Drosophila

TL;DR: It is shown that the function of tinman is required for visceral muscle and heart development, and tinman seems to be one of the earliest genes required for heart development and the first gene reported for which a crucial function in the early mesodermal subdivisions has been implicated.
Journal ArticleDOI

Replication of smooth muscle cells in vascular disease.

TL;DR: This review attempts to consider the current state of knowledge of the mechanisms controlling smooth muscle proliferation in these two diseases, to put that knowledge into the context of what is known about smooth muscle biology, and to offer two hypotheses on the possible roles of smooth muscle developmental biology in manifestations of atherosclerosis and hypertension in adult humans.
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Which marker to follow muscle ligneage in the mouse embryo?

The smooth muscle myosin heavy chain (SM-MHC) is a highly specific marker for the smooth muscle lineage during mouse embryogenesis.