Xiao-Long Kang

Sun Yat-Sen University, Shengcheng, Guangdong, China

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Publications (2)4.14 Total impact

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    ABSTRACT: The purpose of the present study was to compare the differences between the role of volume-regulated Cl(-) channels (VRCCs) in veins and arteries. We used the whole cell patch clamp and fluorescence imaging techniques to evaluate swelling-induced Cl(-) current (I(Cl,vol)) and changes in the intracellular concentrations of Cl(-) ([Cl(-)](i)) induced by hypotonic solutions in rat femoral artery cells (FASMCs) and vein smooth muscle cells (FVSMCs). I(Cl,vol) and [Cl(-)](i) decline induced by hypotonic solution were more prominent in FASMCs than in FVSMCs. I(Cl,vol) and the alterations in [Cl(-)](i) were gradually increased as the number of cell passages increased. However, the regulatory function of tyrosine protein phosphorylation in volume-regulated chloride movement is prominent in veins. The expression of ClC-3 was higher in FASMCs than in FVSMCs. VRCC activity is more pronounced in rat femoral arteries than in veins. VRCC activity and tyrosine protein phosphorylation regulative function increase gradually as vascular cells switch from contractile to proliferative phenotypes.
    Canadian Journal of Physiology and Pharmacology 11/2012; 90(11):1516-26. · 1.56 Impact Factor
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    ABSTRACT: Statins have been demonstrated to effectively inhibit proliferation and induce apoptosis in cancer cells by inhibition of geranylgeranylation, however its novel molecular mechanism remains to be determined. Recently simvastatin has been found to result in the synergistic induction of apoptosis with 7-hydroxystaurosporine (UCN-01) (a Chk1 inhibitor) in myeloma cells. Therefore we hypothesized that Chk1 plays a role in the anti-myeloma effect of simvastatin. Interestingly, we found that simvastatin caused a dose-dependent increase in S phase cell cycle and induced significant apoptosis. The results of western blot showed that simvastatin-induced S-phase cell cycle arrest was associated with activation of Chk1, downregulation of Cdc25A, cyclin A and CDK2 expression. Additionally, simvastatin-induced apoptosis was accompanied by diminished Bcl-2 protein expression, increased cytosolic cytochrome c level, and activation of caspase 9 and caspase 3. Further investigation revealed that silence of Chk1 expression by Chk1 specific siRNA inhibited simvastatin-induced activation of Chk1, downregulation of Cdc25A, cyclin A and CDK2 expression, and diminished S phase cell cycle arrest. Additionally, inhibition of Chk1 expression enhanced simvastatin-induced downregulation of Bcl-2, caspase 9 cleavage and subsequent apoptosis. These results suggested that the Chk1-Cdc25A-cyclin A/CDk2 pathway was involved in simvastatin-induced S-phase cell cycle arrest and apoptosis in multiple myeloma cell lines.
    European journal of pharmacology 09/2011; 670(2-3):356-64. · 2.59 Impact Factor