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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Sci+Rep
2017 ; 7
(ä): 42092
Nephropedia Template TP
Sci Rep
2017[Feb]; 7
(ä): 42092
PMID28191820
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The vascular smooth muscle cells (VSMCs) are exposed to interstitial flow induced
shear stress that may be sensed by the surface glycocalyx, a surface layer
composed primarily of proteoglycans and glycoproteins, to mediate cell
contraction during the myogenic response. We, therefore, attempted to elucidate
the signal pathway of the glycocalyx mechanotransduction in shear stress
regulated SMC contraction. Human umbilical vein SMCs (HUVSMCs) deprived of serum
for 3-4 days were exposed to a step increase (0 to 20?dyn/cm(2)) in shear stress
in a parallel plate flow chamber, and reduction in the cell area was quantified
as contraction. The expressions of Rho kinase (ROCK) and its downstream signal
molecules, the myosin-binding subunit of myosin phosphatase (MYPT) and the myosin
light chain 2 (MLC2), were evaluated. Results showed that the exposure of HUVSMCs
to shear stress for 30?min induced cell contraction significantly, which was
accompanied by ROCK1 up-regulation, re-distribution, as well as MYPT1 and MLC
activation. However, these shear induced phenomenon could be completely abolished
by heparinase III or Y-27632 pre-treatment. These results indicate shear stress
induced VSMC contraction was mediated by cell surface glycocalyx via a ROCK-MLC
phosphatase (MLCP) pathway, providing evidence of the glycocalyx
mechanotransduction in myogenic response.