Proliferation of vascular smooth muscle cells regulated by NO/PKG mediated via Ca~(2+)/calcineurin signaling pathway / 基础医学与临床

ABSTRACT

Objective To study the regulation of VSMC proliferation by NO/PKG via modulating intracellular Ca~(2+)/calcineurin(CaN) signaling pathway.Methods Primary VSMCs from rat aorta were used as the experimental model.CaN protein and its activity were assayed using immunoblotting and free inorganic phosphate content analysis respectively.Growth and viability of cells were determined by MTT assay and acridine orange and ethidium bromide staining.Results The addition of SNAP and Sp-8-pCPT-cGMPS decrease absorbance of cells stimulated by phenylephrine(PE),whereas the addition of Rp-8-pCPT-cGMPS increases it.In SMCs p retreated with Ver,absorbance of cells stimulated by PE decreased and was further inhibited by the additional treatment of SNAP and Sp-8-pCPT-cGMPS.In SMCs pretreated with CsA,absorbance of cells stimulated by PE decrease,but it can not be further altered by the additional treatment of SNAP,Sp-8-pCPT-cGMPS and Rp-8-pCPT-cGMPS.Moreover,expression and activities of CaN induced by PE is inhibited by SNAP and Sp-8-pCPT-cGMPS.Conclusion NO/PKG inhibits the proliferation of vascular SMCs without decreasing cell survival rate,which is mediated via intracellular Ca~(2+)/CaN signaling pathway.