Morphology of vascular smooth muscle cells and pericytes as revealed by transmission and scanning EM

Author(s):  
Y. Uehara ◽  
T. Komuro ◽  
J. Desaki

Although subcellular organization of vascular smooth muscle cells and pericytes have been described by a number of authors, the precise overall structure of these cells has not been revealed at the fine structural level.In order to extend our knowledge in understanding of vascular function, the present paper deals the three dimensional organization of these cells as studied with a transmission EM using serial sections and with a scanning EM using materials from which connective tissue elements are removed.For the reconstruction study, arterioles ranging in diameter from l0um to 25um are selected from the hamster skeletal muscle and the rat pancreas.Fig. 1. demonstrates an example of the reconstructed model of the arteriole smooth muscle cell. Here the muscle cell takes a spiral form which coils nearly twice around the endothelial column. The shape and disposition of the muscle cells gradually become to be irregular towards the capillary bed.

2019 ◽  
Vol 7 (1) ◽  
pp. 347-361 ◽  
Author(s):  
Haishuang Lin ◽  
Qian Du ◽  
Qiang Li ◽  
Ou Wang ◽  
Zhanqi Wang ◽  
...  

3D thermoreversible PNIPAAm-PEG hydrogels are used for scalable production of human pluripotent stem cell-derived vascular smooth muscle cells.


2018 ◽  
Author(s):  
Thomas R. Whitesell ◽  
Paul Chrystal ◽  
Jae-Ryeon Ryu ◽  
Nicole Munsie ◽  
Ann Grosse ◽  
...  

AbstractDespite the critical role of vascular mural cells (smooth muscle cells and pericytes) in supporting the endothelium of blood vessels, we know little of their early morphogenesis and differentiation. foxc1b:EGFP expressing cells in zebrafish associate with the vascular endothelium (kdrl) and co-express a smooth muscle marker (acta2), but not a pericyte marker (pdgfrβ). The expression of foxc1b in early peri-endothelial mesenchymal cells allows us to follow the morphogenesis of mesenchyme into acta2 expressing vascular smooth muscle cells. We show that mural cells expressing different markers associate with vessels of different diameters, depending on their embryonic location and developmental timing, suggesting marker expression is predictive of functional differences. We identify gene expression signatures for an enriched vascular smooth muscle cell population (foxc1b + acta2) and all smooth muscle (acta2) using fluorescence-activated cell sorting and RNA-Seq. Finally, we demonstrate that progressive loss of foxc1a/foxc1b results in decreased smooth muscle cell coverage. Together, our data highlight the early cellular dynamics and transcriptome profiles of smooth muscle cells in vivo, using foxc1b as a unique tool to probe vascular smooth muscle cell differentiation.Summary StatementTracing the morphogenesis and transcriptome of early vascular smooth muscle cells using foxc1b


2000 ◽  
Vol 113 (11) ◽  
pp. 2055-2064
Author(s):  
E. Stringa ◽  
V. Knauper ◽  
G. Murphy ◽  
J. Gavrilovic

Cell migration is a key event in many biological processes and depends on signals from both extracellular matrix and soluble motogenic factors. During atherosclerotic plaque development, vascular smooth muscle cells migrate from the tunica media to the intima through a basement membrane and interstitial collagenous matrix and proliferate to form a neointima. Matrix metalloproteinases have previously been implicated in neointimal formation and in this study smooth muscle cell adhesion and migration on degraded collagen have been evaluated. Vascular smooth muscle cells adhered to native intact collagen type I and to its first degradation by-product, 3/4 fragment (generated by collagenase-3 cleavage), unwound at 35 degrees C to mimic physiological conditions. PDGF-BB pre-treatment induced a fourfold stimulation of smooth muscle cell motility on the collagen 3/4 fragment whereas no increase in smooth muscle cell motility on collagen type I was observed. Cell migration on collagen type I was mediated by alpha2 integrin, whereas PDGF-BB-stimulated migration on the 3/4 collagen fragment was dependent on alphavbeta3 integrin. alphavbeta3 integrin was organised in clusters concentrated at the leading and trailing edges of the cells and was only expressed when cells were exposed to the 3/4 collagen fragment. Tyrphostin A9, an inhibitor of PDGF receptor-beta tyrosine kinase activity, resulted in complete abolition of migration of PDGF-BB treated cells on collagen type I and 3/4 fragment. These results strongly support the hypothesis that the cellular migratory response to soluble motogens can be regulated by proteolytic modification of the extracellular matrix.


2018 ◽  
Author(s):  
Charlene Watterston ◽  
Lei Zeng ◽  
Abidemi Onabadejo ◽  
Sarah J Childs

AbstractVascular smooth muscle cells (vSMC) are essential to the integrity of blood vessels, and therefore an attractive target of therapeutics aimed at improving vascular function. Smooth muscle cells are one of the few cell types that maintain plasticity and can switch phenotypes from differentiated (contractile) to de-differentiated (synthetic) and vice versa. As small regulatory transcripts, miRNAs act as genetic ‘fine tuners’ of posttranscriptional events and can act as genetic switches promoting phenotypic switching. The microRNAmiR26atargets the BMP signalling effector,smad1. We show that loss ofmiR26leads to hemorrhage (a loss of vascular stability)in vivo, suggesting altered vascular differentiation. Reduction inmiR26alevels increasessmad1mRNA and phospho-Smad1 (pSmad1) levels. We show that increasing BMP signalling by overexpression ofsmad1also leads to hemorrhage and that normalization of Smad1 levels through double knockdown ofmiR26andsmad1rescues hemorrhage suggesting a direct relationship betweenmiR26andsmad1and vascular stability. Using a BMP genetic reporter and pSmad1 staining we show that the effect ofmiR26on vascular instability is non-autonomous; BMP signalling is active in embryonic endothelial cells, but not in smooth muscle cells. Nonetheless, increased BMP signalling due to loss ofmiR26results in an increase inacta2-expressing smooth muscle cell numbers and promotes a differentiated smooth muscle morphology. Taken together our data suggests thatmiR26modulates BMP signalling in endothelial cells and indirectly promotes a differentiated smooth muscle phenotype. Our data also suggests that crosstalk from BMP-responsive endothelium to smooth muscle is important for its differentiation.


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