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[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].
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[This corrects the article DOI: 10.1016/j.apsb.2021.04.013.].
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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
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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.
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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.
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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).
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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.
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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.
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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.
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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.
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The effects of drugs on intracellular calcium concentration(［Ca2+］i) were investigated with fura-2 fluorescence technique to investigate ATP and thrombin-induced Ca2+ entry in bovine aortic endothelial cells(BAEC). It was found that application of ATP and thrombin gave rise to biphasic ［Ca2+］i elevation. ATP or thrombin only triggered a fraction of cyclopiazonic acid(CPA)-sensitive Ca2+ store, which was enough to activate Ca2+ entry. The Ca2+ release induced by thrombin resulted from the activation of phospholipase C(PLC), whereas the PLC-independent mechanism was involved in ATP-induced Ca2+ release. Nifedipine had no effect on ATP and thrombin- induced Ca2+ entry. SK&F 96365 and ginsenoside-2A inhibited both ATP and CPA-induced Ca2+ entry, however no effect of them on thrombin-induced Ca2+ entry was found. The inhibitory effects of SK&F 96365 and ginsenoside-2A on CPA-induced Ca2+ entry were less than that on ATP-induced Ca2+ entry. The Ca2+ influx sensitive to SK&F 96365 was not the same as that to ginsenoside-2A. These observations suggest that both ATP and thrombin evoke Ca2+ release and Ca2+ influx by activation of different receptor. However their mechanisms appear different.
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AIM: To investigate the relationship between chloride channels and the Ca 2+influx induced by adrendine(Adr). METHODS: The effects of drugs on Adr-induced Ca 2+influx were investigated with Fura-2 fluorescence technique. RESULTS: Adr-induced Ca 2+influx was inhibited by nifedipine,SK&F96365,NFA and furosemide in a concentration manner respectively; Ca 2+influx could be further inhibited by NFA or furosemide after the maximal inhibition by SK&F96365;SK&F96365 also could further inhibit the Ca 2+influx which had been inhibited by NFA or furosemide. Genistein and vanadate could reduce or increase the Ca 2+influx respectively. CONCLUSION: Ca 2+influx induced by Adr is related to VDC and ROC, and chloride channels involves in the processes.The levels of tyrosine phosphoralation affect the Ca 2+influx.
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Endothelium-derived hyperpolarizing factor (EDHF) is the third factor released by en-dothelial cell other than NO and PGI2. It relaxes smooth muscle accompanied by a hyperpolarization in the membrane potential. EDHF may be epoxye-icosatrienoic acids (EETs) formed from arachidon-ic acid by the action of cytochrome P450. It is synthesized and/or released by endothelial cell as a result of an cytosolic Ca2+ increase, which is stimulated by the action of acetylcholine or bradykinin on endothelial cell. EDHF is shown to activate Ca2+-activated K+ channels and induce a hyperpolarization in the membrane potential in vascular smooth muscle. The hyperpolarization of the membrane inhibits the opening of voltage-dependentcalcium channels, allows calcium sequestration and removal mechanisms to lower intracellular calcium, and leads smooth muscle to relaxation. In large conducing arteries, EDHF may provide a secondary system to NO, which assumes primary importance in endothelium-dependent relaxation and inhibits the release of EDHF. However, in small resistance arteries, EDHF appears to be a major determinant of vascular calibre, and may be of primary importance in the regulation of vascular resistance.
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The effects of Panax notoginsen saponins ( PNGS ) on myocar- dial ischemia and reperfusion injury in conscious rabbit were studied with observation of changes in electrocardiogram (ECG), the activities of creatine phosphokinase ( CPK ) and lactate dehydrogen-ase ( LD ) and the size of ischemic area. 50 mg/kg and 100 mg/kg PNGS significantly decreased the activities of CPK and LD, and the abnormal changes of ECG during ischemic and reperfusion periods. Also, PNGS significantly reduced the size of myocardial ischemic area. These results suggest that PNGS have the protective effects on myocardial ischemia and reperfusion injury.
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The effect of the total saponins of panax notogiseng ( PNS ) on transmitter release was studied on mouse diaphragm. The Ca2+ -mediated release evoked by electric stimulation at the nerve terminal or by raised K+ level was markedly reduced by Cd2 + , but not affected by PNS & nifedipine. Also, PNS didn't change the basic frequency of mepp & the Ba2+ entry during depolarization of the terminal. C-ompared with PNS, Cd2 had a significant effect on decreasing Ba2+ entry. These results suggest that PNS can not change spontanous, synchronous or asynchronous release, the Ca2+ channel involved in the transmitter release at the mouse motor nerve terminal belongs in N type Ca2 channel.
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AIM To study the effects of protein tyrosine kinase inhibitor and protein tyrosine phosphatase inhibitor on cultured bovine cerebrovascular smooth muscle cells (CSMC) Ca 2+ store operated Ca 2+ influx. METHODS Cell culture and single intracellular free Ca 2+ concentration was measured in fura 2/Am flueorescence probe by MetaFluor Fluorescence ratio imaging system. RESULTS (1) protein tyrosine kinase inhibitor (genistein,2.5,5,10 ?mol?L -1 )decreased Ca 2+ influx significantly induced by endothelin 1(ET 1),ATP,cyclopiazonic acid(CPA) in concentration dependent manner; (2) Protein tyrosine phosphatase inhibitor (vanadate,2,4,8 ?mol?L -1 ) increased Ca 2+ influx significantly induced by ET 1,ATP,CPA in concentration dependent manner. CONCLUSION Protein tyrosine kinase inhibitor and protein tyrosine phosphatase inhibitor have effects on Ca 2+ store operated Ca 2+ influx induced by ET 1, ATP, CPA. Protein tyrosine phosphorylation participats in the signal transduction of Ca 2+ store operat Ca 2+ influx in cerebrovascular smooth muscle cells.
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AIM To study the effects of endothelin 1(ET 1) on ClC 3 chloride channel protein expression in cultured bovine cerebrovascular smooth muscle cells (CSMC). METHODS Cell culture and Western blot. RESULTS ① The endogenous ClC 3 expression was found in basilar artery, middle cerebral artery, and microvessel; ② The molecular weight of expressed ClC 3 chloride channel protein was about 95 ku; ③ ET 1 enhanced ClC 3 protein expression which was inhibited by nifedipine and SK&F96365. Cyclopiazonic acid(CPA) increased the expression of ClC 3 protein in a concentration dependant manner, and enhanced ET 1 effect on this protein expression. CONCLUSION ET 1 stimulated ClC 3 chloride channel protein expression in cultured bovine cerebrovascular smooth muscle cells. The intracellular Ca 2+ plays an important role on signal transduction pathway in ClC 3 protein expression process.
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AIM To study the effects of different kinds of chloride channel blockers on KCl and 5 HT induced contractile responses in cerebrovascular smooth muscle. METHOD The tension of rabbit basilar artery rings was measured. RESULTS ① DIDS, furosemide and NPPB inhibited the responses to KCl and 5 HT in a concentration dependent manner. The effects of DIDS, furosemide and NPPB on the response to 5 HT were stronger than that to KCl. ②When SK&F 96365 evoked a maximum inhibitory effect on 5 HT induced response, subsequent additions of DIDS, furosemide and NPPB could further produced vascular relaxation. CONCLUSION The chloride channel participates KCl and 5 HT induced contractile responses in cerebral basilar artery.
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AIM To investigate the role of Trp3 in the Ca 2+ influx induced by ? 1B AR in HEK293 cells and the effect of tyrosine kinase on it. METHODS With lipofect AMINE2000 reagent, hTrp3 cDNA was transfected to HEK293 cells and ? 1B HEK293 cells respectively. The expression of Trp3 was examined by Western blot. With Fura 2/AM spectrophoto fluorometry, Ca 2+ influx was determined. RESULTS HTrp3 was expressed endogenously in HEK293 cells, and the expression increased in hTrp3 transfected cells. Compared with untransfected cells, transfection of hTrp3 cDNA increased Ca 2+ influx induced by ? 1B AR ( P 0 05). 5～30 ?mol?L -1 genistein inhibited Ca 2+ influx induced by ? 1B AR in hTrp3 cDNA transfected cells and the maximum inhibitory rate was (75 2?12 6)% . CONCLUSION Transfection of hTrp3 cDNA increased Ca 2+ influx induced by ? 1B AR in HEK293 cells. This process was regulated by tyrosine kinase.
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AIM To investigate the roles of Cl- channels in Ca2+ influx induced by activaion of al- adrenoceptor subtypes in transfected-CHO cells. METHODS The effects of drugs on ?1A、?1B and ?1D- AR-induced Ca2+ influx were investigated with Fura2 fluorescence technique. RESULTS The ?1A-AR- induced Ca2+ influx was inhibited by furosemide(2 .5 ~ 10 M?mol?L- 1 )and SK&F96365(5- 15 ?mol?L- 1 ) in a concentration- dependent manner respectively; The ?1B-AR-induced Ca2+ influx could also be inhibit inhibited by NFA(2. 5 ~ 10 ?mol? L-1 ), whereas the alD AR-induced Ca2+ influx was only suppressed by NFA. In ?1B-CHO cells, Adr-triggered Ca2+ influx could be further inhibited by NFA or furosemide after the maximal inhibition by SK&F96365;SK&F96365 could further inhibit Ca2+ influx which had been inhibited by NFA or furosemide. In ?1A-CHO cells, Adr-triggered Ca2+ influx could be further inhibited by SK&F96365 after had been inhibited by furosemide; furosemide could not further inhibite Ca2+ influx which had been inhibited by S&F96365. CONCLUSION There are different characteristics of CI- channels related to ?1A、 ?1B and ?1D-AR-induced Ca2+ influx.