scholarly journals Collagen degradation and platelet-derived growth factor stimulate the migration of vascular smooth muscle cells

2000 ◽  
Vol 113 (11) ◽  
pp. 2055-2064
Author(s):  
E. Stringa ◽  
V. Knauper ◽  
G. Murphy ◽  
J. Gavrilovic
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I

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.

scholarly journals An In situ Collagen-HA Hydrogel System Promotes Survival and Preserves the Proangiogenic Secretion of hiPSC-derived Vascular Smooth Muscle Cells

2020 ◽  
Author(s):  
Biraja C. Dash ◽  
Kaiti Duan ◽  
Hao Xing ◽  
Themis R. Kyriakides ◽  
Henry C. Hsia
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Collagen Type ◽  
Muscle Cells ◽  
Collagen Type I ◽  
Type I ◽  
Hydrogel System

AbstractHuman induced pluripotent stem cell-derived vascular smooth muscle cells (hiPSC-VSMCs) with proangiogenic properties have huge therapeutic potential. While hiPSC-VSMCs have already been utilized for wound healing using a biomimetic collagen scaffold, an in situ forming hydrogel mimicking the native environment of skin offers the promise of hiPSC-VSMC mediated repair and regeneration. Herein, the impact of a collagen type-I-hyaluronic acid (HA) in situ hydrogel cross-linked using a PEG-based cross-linker on hiPSC-VSMCs viability and proangiogenic paracrine secretion was investigated. Our study demonstrated increases in cell viability, maintenance of phenotype and proangiogenic growth factor secretion, and proangiogenic activity in response to the conditioned medium. The optimally cross-linked and functionalized collagen type-I/HA hydrogel system developed in this study shows promise as an in situ hiPSC-VSMC carrier system for wound regeneration.

scholarly journals Morphogenesis and differentiation of embryonic vascular smooth muscle cells in zebrafish

2018 ◽  
Author(s):  
Thomas R. Whitesell ◽  
Paul Chrystal ◽  
Jae-Ryeon Ryu ◽  
Nicole Munsie ◽  
Ann Grosse ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Critical Role ◽  
Muscle Cells ◽  
Mural Cells

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

scholarly journals Downregulation of miRNA-1-3p modulates cyclic stretch-mediated proliferation of vascular smooth muscle cells through regulation of ETS-1

2020 ◽  
Vol 72 (4) ◽  
pp. 587-598
Author(s):  
Xizhen Wang ◽  
Aihua Li ◽  
Ruikang Duan ◽  
Bin Zhang
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Collagen Type ◽  
Muscle Cells ◽  
Mechanical Stretch ◽  
Cyclic Stretch ◽  
Luciferase Reporter ◽  
Type I

Mechanical stretch modulates the proliferation of vascular smooth muscle cells (VSMCs) and plays an important role in the pathogenesis of hypertension, but the underlying mechanisms are unclear. We investigated the role of microRNA- 1-3p (miRNA-1-3p) on the proliferation of VSMCs induced by mechanical cyclic stretch. Our data show that miRNA-1-3p is downregulated in the aorta of the spontaneous hypertension rat (SHR). Pathological mechanical stretch at 15% suppressed the expression of miRNA-1-3p, calponin and SM22, but enhanced the proliferation of VSMCs as well as the expression of the V-ets erythroblastosis virus E26 oncogene homolog 1 (ETS-1), collagen type I alpha (Col-1a), collagen type III alpha (Col-3a) and elastin. Overexpression of miRNA-1-3p inhibited cell proliferation and induced the expression of calponin and SM22, but decreased the expression of ETS-1, Col-1a, Col-3a and elastin. Mechanical stretch at 15% combined with losartan treatment increased the expression of miRNA-1-3p, calponin and SM22, and decreased the expression of ETS-1, Col-1a and Col-3a. Dual luciferase reporter assays revealed ETS-1 as a direct target of miRNA-1-3p. These findings suggest that miRNA-1-3p regulates VSMC function through ETS-1 regulation during hypertension-induced vascular remodeling. MiRNA-1-3p may be a viable therapeutic target for hypertension.

Protein Kinase C Delta Is Necessary for the secretion of Collagen Type I from Vascular Smooth Muscle Cells

2008 ◽  
Vol 22 (S2) ◽  
pp. 609-609
Author(s):  
Andrew Zohlman ◽  
Kentaro Kamiya ◽  
Kaori Kato ◽  
Susana B Salvarezza ◽  
Stephen B Doty ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Kinase C

scholarly journals Involvement of DHX9/YB-1 complex induced alternative splicing of Krüppel-like factor 5 mRNA in phenotypic transformation of vascular smooth muscle cells

2019 ◽  
Vol 317 (2) ◽  
pp. C262-C269
Author(s):  
Wei Huan ◽  
Jing Zhang ◽  
Yingke Li ◽  
Kangkang Zhi
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Alternative Splicing ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cell ◽  
Muscle Cells ◽  
Phenotypic Transformation

Phenotypic transformation of vascular smooth muscle cells is a key phenomenon in the development of aortic dissection disease. However, the molecular mechanisms underlying this phenomenon have not been fully understood. We used β-BAPN combined with ANG II treatment to establish a disease model of acute aortic dissection (AAD) in mice. We first examined the gene expression profile of aortic tissue in mice with AAD using a gene chip, followed by confirmation of DExH-box helicase 9 (DHX9) expression using RT-PCR, Western blot, and immunofluorescence analysis. We further developed vascular smooth muscle cell-specific DHX9 conditional knockout mice and conducted differential and functional analysis of gene expression and alternative splicing in mouse vascular smooth muscle cells. Finally, we examined the involvement of DHX9 in Krüppel-like factor 5 ( KLF5) mRNA alternative splicing. Our study reported a significant decrease in the expression of DHX9 in the vascular smooth muscle cells (VSMCs) of mice with AAD. The smooth muscle cell-specific knockout of DHX9 exacerbated the development of AAD and altered the transcriptional level expression of many smooth muscle cell phenotype-related genes. Finally, we reported that DHX9 may induce alternative splicing of KLF5 mRNA by bridging YB-1. These results together suggested a new pathogenic mechanism underlying the development of AAD, and future research of this mechanism may help identify effective therapeutic intervention for AAD.

Sin3B mediates collagen type I gene repression by interferon gamma in vascular smooth muscle cells

2014 ◽  
Vol 447 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Xinyu Weng ◽  
Xian Cheng ◽  
Xiaoyan Wu ◽  
Huihui Xu ◽  
Mingming Fang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Interferon Gamma ◽  
Collagen Type ◽  
Collagen Type I ◽  
Gene Repression ◽  
Type I ◽  
I Gene
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