scholarly journals Cyclic stretch-induced thrombin generation by rat vascular smooth muscle cells is mediated by the integrin αvβ3 pathway

2012 ◽  
Vol 96 (3) ◽  
pp. 513-523 ◽  
Author(s):  
Xianqing Mao ◽  
Rose Said ◽  
Huguette Louis ◽  
Jean-Pierre Max ◽  
Mustapha Bourhim ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Thrombin Generation ◽  
Integrin Αvβ3 ◽  
Muscle Cells ◽  
Cyclic Stretch

scholarly journals The involvement of aldosterone in cyclic stretch-mediated activation of NADPH oxidase in vascular smooth muscle cells

2009 ◽  
Vol 32 (8) ◽  
pp. 690-699 ◽  
Author(s):  
Takahiro Ohmine ◽  
Yoshikazu Miwa ◽  
Fumi Takahashi-Yanaga ◽  
Sachio Morimoto ◽  
Yoshihiko Maehara ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Nadph Oxidase ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cyclic Stretch

scholarly journals SIRT1 and FOXO Mediate Contractile Differentiation of Vascular Smooth Muscle Cells under Cyclic Stretch

2015 ◽  
Vol 37 (5) ◽  
pp. 1817-1829 ◽  
Author(s):  
Kai Huang ◽  
Zhi-Qiang Yan ◽  
Dan Zhao ◽  
Si-Guo Chen ◽  
Li-Zhi Gao ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Mechanical Stretch ◽  
Cyclic Stretch ◽  
Underlying Mechanisms

Background/Aims: Physiological mechanical stretch in vivo helps to maintain the quiescent contractile differentiation of vascular smooth muscle cells (VSMCs), but the underlying mechanisms are still unclear. Here, we investigated the effects of SIRT1 in VSMC differentiation in response to mechanical cyclic stretch. Methods and Results: Rat VSMCs were subjected to 10%-1.25Hz-cyclic stretch in vitro using a FX-4000T system. The data indicated that the expression of contractile markers, including α-actin, calponin and SM22α, was significantly enhanced in VSMCs that were subjected to cyclic stretch compared to the static controls. The expression of SIRT1 and FOXO3a was increased by the stretch, but the expression of FOXO4 was decreased. Decreasing SIRT1 by siRNA transfection attenuated the stretch-induced expression of contractile VSMC markers and FOXO3a. Furthermore, increasing SIRT1 by either treatment with activator resveratrol or transfection with a plasmid to induce overexpression increased the expression of FOXO3a and contractile markers, and decreased the expression of FOXO4 in VSMCs. Similar trends were observed in VSMCs of SIRT1 (+/-) knockout mice. The overexpression of FOXO3a promoted the expression of contractile markers in VSMCs, while the overexpression of FOXO4 demonstrated the opposite effect. Conclusion: Our results indicated that physiological cyclic stretch promotes the contractile differentiation of VSMCs via the SIRT1/FOXO pathways and thus contributes to maintaining vascular homeostasis.

Temporal phosphoproteomics to investigate the mechanotransduction of vascular smooth muscle cells in response to cyclic stretch

2014 ◽  
Vol 47 (15) ◽  
pp. 3622-3629 ◽  
Author(s):  
Yu-Chen Yang ◽  
Xiao-Dong Wang ◽  
Kai Huang ◽  
Lu Wang ◽  
Zong-Lai Jiang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cyclic Stretch

scholarly journals Peri/epicellular protein disulfide isomerase-A1 acts as an upstream organizer of cytoskeletal mechanoadaptation in vascular smooth muscle cells

2019 ◽  
Vol 316 (3) ◽  
pp. H566-H579 ◽  
Author(s):  
Leonardo Y. Tanaka ◽  
Thaís L. S. Araujo ◽  
Andres I. Rodriguez ◽  
Mariana S. Ferraz ◽  
Vitor B. Pelegati ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Protein Disulfide Isomerase ◽  
Traction Force ◽  
Muscle Cells ◽  
Cyclic Stretch ◽  
Disulfide Isomerase ◽  
Protein Disulfide

Although redox processes closely interplay with mechanoresponses to control vascular remodeling, redox pathways coupling mechanostimulation to cellular cytoskeletal organization remain unclear. The peri/epicellular pool of protein disulfide isomerase-A1 (pecPDIA1) supports postinjury vessel remodeling. Using distinct models, we investigated whether pecPDIA1 could work as a redox-dependent organizer of cytoskeletal mechanoresponses. In vascular smooth muscle cells (VSMCs), pecPDIA1 immunoneutralization impaired stress fiber assembly in response to equibiaxial stretch and, under uniaxial stretch, significantly perturbed cell repositioning perpendicularly to stretch orientation. During cyclic stretch, pecPDIA1 supported thiol oxidation of the known mechanosensor β1-integrin and promoted polarized compartmentalization of sulfenylated proteins. Using traction force microscopy, we showed that pecPDIA1 organizes intracellular force distribution. The net contractile moment ratio of platelet-derived growth factor-exposed to basal VSMCs decreased from 0.90 ± 0.09 (IgG-exposed controls) to 0.70 ± 0.08 after pecPDI neutralization ( P < 0.05), together with an enhanced coefficient of variation for distribution of force modules, suggesting increased noise. Moreover, in a single cell model, pecPDIA1 neutralization impaired migration persistence without affecting total distance or velocity, whereas siRNA-mediated total PDIA1 silencing disabled all such variables of VSMC migration. Neither expression nor total activity of the master mechanotransmitter/regulator RhoA was affected by pecPDIA1 neutralization. However, cyclic stretch-induced focal distribution of membrane-bound RhoA was disrupted by pecPDI inhibition, which promoted a nonpolarized pattern of RhoA/caveolin-3 cluster colocalization. Accordingly, FRET biosensors showed that pecPDIA1 supports localized RhoA activity at cell protrusions versus perinuclear regions. Thus, pecPDI acts as a thiol redox-dependent organizer and noise reducer mechanism of cytoskeletal repositioning, oxidant generation, and localized RhoA activation during a variety of VSMC mechanoresponses. NEW & NOTEWORTHY Effects of a peri/epicellular pool of protein disulfide isomerase-A1 (pecPDIA1) during mechanoregulation in vascular smooth muscle cells (VSMCs) were highlighted using approaches such as equibiaxial and uniaxial stretch, random single cell migration, and traction force microscopy. pecPDIA1 regulates organization of the cytoskeleton and minimizes the noise of cell alignment, migration directionality, and persistence. pecPDIA1 mechanisms involve redox control of β1-integrin and localized RhoA activation. pecPDIA1 acts as a novel organizer of mechanoadaptation responses in VSMCs.

scholarly journals Molecular Mechanism of Fibronectin Gene Activation by Cyclic Stretch in Vascular Smooth Muscle Cells

2000 ◽  
Vol 275 (44) ◽  
pp. 34619-34627 ◽  
Author(s):  
Kouichi Tamura ◽  
Yuqing E. Chen ◽  
Marco Lopez-Ilasaca ◽  
Laurent Daviet ◽  
Nobuko Tamura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Molecular Mechanism ◽  
Vascular Smooth Muscle Cells ◽  
Gene Activation ◽  
Muscle Cells ◽  
Cyclic Stretch

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.

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