[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].

[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].

Vascular smooth muscle cell (VSMC) migration plays a critical role in the pathogenesis of many cardiovascular diseases. We recently showed that TMEM16A is involved in hypertension-induced cerebrovascular remodeling. However, it is unclear whether this effect is related to the regulation of VSMC migration. Here, we investigated whether and how TMEM16A contributes to migration in basilar artery smooth muscle cells (BASMCs). We observed that AngII increased the migration of cultured BASMCs, which was markedly inhibited by overexpression of TMEM16A. TMEM16A overexpression inhibited AngII-induced RhoA/ROCK2 activation, and myosin light chain phosphatase (MLCP) and myosin light chain (MLC20) phosphorylation. But AngII-induced myosin light chain kinase (MLCK) activation was not affected by TMEM16A. Furthermore, a suppressed activation of integrin

Volume regulated chloride channel (VRCC) enhances cell proliferation through PI3K/Akt signal pathway ,and inhibits cell apoptosis through mitochondrial pathway in vascular smooth muscle cells ,and accelerates the process of atherosclerosis through JNK/p38 MAPK signal pathway,resulting in increasing SR-A expression and ox-LDL uptake. Cerebrovascular remodeling is mediated by VRCC. This effect of VRCC on remodeling is related to accelerating cell proliferation ,migration and accumulation of. extracellular matrix. As to the molecular identification of VRCC ,it is very complex. VRCC is diversity in various cells or tissues , rather than a single ubiquitous channel,VRCC may be contain variedcell type-or tissue-specific subunitcompositions. ClC-3 volume regulated Cl-channel is regulated by both integrin-Src and Rho/RhA-Rock signal pathways.

0.05).SK & F96365 at the concentration of 5～20 ?mol?L-1 inhibited the Ca2+ influx induced by 1.0 ?mol?L-1 Thapsigargin in a concentration-dependent manner.The inhibitory effect of SK & F96365 on Ca2+ influx was decreased by overexpression of ClC-3 protein.Conclusion ClC-3 chloride channel was involved in the regulation of store-operated Ca2+ entry(SOCE).

Pleiotropic effects of a drug are actions other than that for which the agents were developed.These effects may be desired or undesired,and may be unrelated to their primary mechanism.Statins were designed as a drug for reducing cholesterol,but now pleiotropic effect are found including improvement of endothelial dysfunction,inhancement of eNOS bioavailability antioxide effect,antiinflammatory properties and reduction of hypertension.Understanding those effects is important for treatment and prevention of cardiovascular disease.

Aim To investigate change in Cl- channels of hypertensive rats aortic smooth muscle cells. Methods 2 kidney-2 clip renovascular hypertensive rats(RVHR) model was established. In thoracic aorta smooth muscles from the hypertensive rats 1～12 weeks after operation,the changes of tension of aortic rings were recorded in vitro. Effects of Cl- channel blookers,DIDS(4,4-diisothiocyanato-stilbene-2,2'disulphonate)and NPPB[5-nitro-2-(3-phenylpropy-lamino) benzonic acid], in different concentration on contractile response of hypertensive rats aorta smooth muscle induced by 10 ?mol?L -1 phenylephrine were observed.Results The difference of inhibitory effects of 300 ?mol?L -1 DIDS and 100 ?mol?L -1 NPPB on Phe-induced contractile response between RVHR and sham-operated rats was not evident.Inhibitory effects of 300 ?mol?L -1 DIDS and 100 ?mol?L -1 NPPB on contractile response of hypertensive rats aorta smooth muscle induced by 10 ?mol?L -1 phenylephrine were lower than those of sham-operated rats in 8 weeks and 12 weeks after operation. With extension of time after operation and gradual increase of blood pressure in RVHR,inhibitory effects of DIDS and NPPB on Phe-induced contractile response gradually reduced.Conclusion Action of DIDS-sensitive and NPPB-sensitive Cl- channels in hypertensive rats aortic vascular smooth muscle cells changes. DIDS-sensitive and NPPB-sensitive Cl- channels play an important role in development and maintenance of hypertension.

Acid-sensing ion channels( ASICs )are ubiquitously expressed both in periphery nervous system, where they are involved in nociception,mechanosensation,inflammation ,cardiac angina, and in central nervous system,where they are essential to a variety of physiologic and pathophysiologic processes,such as synaptic plasticity ,learning ,memory and ischemic brain injury. Here in the article, we present a collection of key points about ASICs, ranging from molecular identity and expression, regulatory mechanisms responsible for channel gating to their multiple functions. Finally, a future prospect for the investigation of ASICs is outlined.

Myocardial hypertrophy is the complication of many cardiovascular diseases that induce cardiac remodeling.The molecular mechanism of cardiac remodeling involves abnormal changes in various transmembrane ionic currents in the heart.Recent studies suggest the potential involvement of volume-regulated Cl-current(ICl.Vol)in cardiac hypertrophy.Although the molecular basis of ICl.Vol remains to be elucidated,recent progress is reviewed in the potential role of ICl.Vol in cardiac remodeling.

Aim To investigate the method of cell culture for smooth muscle cells from rat cerebral basilar artery and understand cells growth and biological characteristics.Methods The explant attached method was applied for cell culture of rat basilar artery smooth muscle cells(BASMCs).The cultured BASMCs were identified by immunocytochemical staining.The activities of cells were indicated by the dynamic changes of intracellular calcium concentration observed by RF-5 000 fluorospectro-photometer.Results BASMCs grew out of tissue blocks by 5 days,reached confluency could be subcultured after 2 weeks.Cultured cells were identified by intensely positive immunocytochemical staining to smooth muscle actin-specific.Introduction of calcium channel agonists induced significant increase in Fura-2 fluorescence ratio(F340/F380)and cells were in good condiction.Conclusion Explant attached method is simple,efficient and economic.It provides an ideal cell model for the study of pathogenesis of the cerebral vascular diseases.