Identification of Integrins Involved in Cell Adhesion to Native and Denatured Type I Collagens and the Phenotypic Transition of Rabbit Arterial Smooth Muscle Cells

1995 ◽  
Vol 219 (1) ◽  
pp. 249-256 ◽  
Author(s):  
Mari Yamamoto ◽  
Masayuki Yamato ◽  
Masaru Aoyagi ◽  
Kiyotaka Yamamoto
Keyword(s):  
Smooth Muscle ◽  
Cell Adhesion ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Type I ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells ◽  
Phenotypic Transition

scholarly journals Overexpression of Decorin by Rat Arterial Smooth Muscle Cells Enhances Contraction of Type I Collagen In Vitro

2004 ◽  
Vol 24 (1) ◽  
pp. 67-72 ◽  
Author(s):  
Hannu Järveläinen ◽  
Robert B. Vernon ◽  
Michel D. Gooden ◽  
Aleksandar Francki ◽  
Stephanie Lara ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Type I Collagen ◽  
Muscle Cells ◽  
Type I ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells

scholarly journals Inhibitory effects of growth differentiation factor 11 on autophagy deficiency-induced dedifferentiation of arterial smooth muscle cells

2019 ◽  
Vol 316 (2) ◽  
pp. H345-H356 ◽  
Author(s):  
Xinxu Yuan ◽  
Owais M. Bhat ◽  
Hannah Lohner ◽  
Ningjun Li ◽  
Yang Zhang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Nuclear Antigen ◽  
Inhibitory Effects ◽  
Arterial Smooth Muscle ◽  
Differentiation Factor ◽  
Arterial Smooth Muscle Cells ◽  
Phenotypic Transition ◽  
Carotid Arterial

Growth differentiation factor (GDF)11 has been reported to reverse age-related cardiac hypertrophy in mice and cause youthful regeneration of cardiomyocytes. The present study attempted to test a hypothesis that GDF11 counteracts the pathologic dedifferentiation of mouse carotid arterial smooth muscle cells (CASMCs) due to deficient autophagy. By real-time RT-PCR and Western blot analysis, exogenously administrated GDF11 was found to promote CASMC differentiation with increased expression of various differentiation markers (α-smooth muscle actin, myogenin, myogenic differentiation, and myosin heavy chain) as well as decreased expression of dedifferentiation markers (vimentin and proliferating cell nuclear antigen). Upregulation of the GDF11 gene by trichostatin A (TSA) or CRISPR-cas9 activating plasmids also stimulated the differentiation of CASMCs. Either GDF11 or TSA treatment blocked 7-ketocholesterol-induced CASMC dedifferentiation and autophagosome accumulation as well as lysosome inhibitor bafilomycin-induced dedifferentiation and autophagosome accumulation. Moreover, in CASMCs from mice lacking the CD38 gene, an autophagy deficiency model in CASMCs, GDF11 also inhibited its phenotypic transition to dedifferentiation status. Correspondingly, TSA treatment was shown to decrease GDF11 expression and reverse CASMC dedifferentiation in the partial ligated carotid artery of mice. The inhibitory effects of TSA on dedifferentiation of CASMCs were accompanied by reduced autophagosome accumulation in the arterial wall, which was accompanied by attenuated neointima formation in partial ligated carotid arteries. We concluded that GDF11 promotes CASMC differentiation and prevents the phenotypic transition of these cells induced by autophagosome accumulation during different pathological stimulations, such as Western diet, lysosome function deficiency, and inflammation.NEW & NOTEWORTHY The present study demonstrates that growth differentiation factor (GDF)11 promotes autophagy and subsequent differentiation in carotid arterial smooth muscle cells. Upregulation of GDF11 counteracts dedifferentiation under different pathological conditions. These findings provide novel insights into the regulatory role of GDF11 in the counteracting of sclerotic arterial diseases and also suggest that activation or induction of GDF11 may be a new therapeutic strategy for the treatment or prevention of these diseases.

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