Abstract
Neferine inhibits the angiotensin II (AngII)-induced proliferation of vascular smooth muscle cells (SMCs), but the underlying mechanism is unclear. The aim of this study was to explore the mechanism underlying the effect of neferine on the proliferation of vascular SMCs. Rat aortic SMCs (RASMCs) were used and fractalkine (Fkn) gene expression was measured by quantitative polymerase chain reaction and western blot analysis. The proliferation of RASMCs was analyzed by MTT assay and flow cytometry. It was revealed that AngII induced Fkn expression in a dose- and time-dependent manner. Fkn-knockdown with small interfering RNA attenuated the AngII-induced RASMC proliferation. Furthermore, neferine inhibited Fkn expression and attenuated the AngII-induced RASMC proliferation. These findings suggest that the Fkn gene may play an important role in AngII-induced RASMC proliferation and that neferine acts to attenuate AngII-induced RASMC proliferation by inhibiting Fkn expression.
Highlights
The proliferation of smooth muscle cells (SMCs) plays a pivotal role in cardiovascular diseases [1,2,3]
MTT assay showed that angiotensin II (AngII) could promote Rat aortic SMCs (RASMCs) proliferation in a time‐ and concentration‐dependent manner (P
The following observations were noted: i) AngII stimulated Fkn expression in RASMCs; ii) Fkn gene‐knockdown attenuated the AngII‐induced proliferation of RASMCs and iii) neferine inhibited AngII‐induced Fkn expression, attenuating the proliferative effect of AngII on RASMCs
Summary
The proliferation of smooth muscle cells (SMCs) plays a pivotal role in cardiovascular diseases [1,2,3]. Sullivan et al [13] found that the expression of Fkn was markedly increased in the mesenteric arteries of spontaneously hypertensive rats (SHRs) and was notably higher in female SHRs. Studies have demonstrated that Fkn can induce SMC proliferation, which is mediated by nuclear factor κB‐dependent inflammatory signals [14,15]. Rius et al [16] found that by stimulating endothelial cells with 1 μmol/l AngII, Fkn expression was upregulated in the cells. These findings highlight the significance of Fkn in the pathogenesis of hypertension and suggest it may play a role in vascular remodeling
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