中国血液流变学杂志
中國血液流變學雜誌
중국혈액류변학잡지
CHINESE JOURNAL OF HEMORHEOLOGY
2013年
2期
226-228
,共3页
曹学照%艾春雨%刘钢%马虹
曹學照%艾春雨%劉鋼%馬虹
조학조%애춘우%류강%마홍
肾素前体%ERK1/2%Akt%大鼠血管平滑肌细胞
腎素前體%ERK1/2%Akt%大鼠血管平滑肌細胞
신소전체%ERK1/2%Akt%대서혈관평활기세포
prorenin%ERK1/2%Akt%vascular smooth muscle cell
目的探讨肾素前体(prorenin)诱导大鼠血管平滑肌细胞的增殖是否通过ERK1/2和Akt通路。方法利用[3H]同位素标记的胸苷的结合检测血管平滑肌细胞增殖。蛋白印记分析检测肾素前体诱导的平滑肌细胞ERK和Akt的活化。结果肾素前体剂量依赖性诱导ERK和Akt磷酸化,在20min达到高峰。20nmol/L肾素前体处理细胞48h后细胞内[3H]同位素标记的胸苷含量增多(P<0.05),这种促进细胞增殖的作用可以被预处理ERK激酶抑制剂PD98059(100μmol/L)和PI3K激酶抑制剂wortmannin(100nmol/L)阻断。结论实验结果表明肾素前体诱导血管平滑肌细胞产生的增殖是通过ERK1/2和Akt通路发挥作用。
目的探討腎素前體(prorenin)誘導大鼠血管平滑肌細胞的增殖是否通過ERK1/2和Akt通路。方法利用[3H]同位素標記的胸苷的結閤檢測血管平滑肌細胞增殖。蛋白印記分析檢測腎素前體誘導的平滑肌細胞ERK和Akt的活化。結果腎素前體劑量依賴性誘導ERK和Akt燐痠化,在20min達到高峰。20nmol/L腎素前體處理細胞48h後細胞內[3H]同位素標記的胸苷含量增多(P<0.05),這種促進細胞增殖的作用可以被預處理ERK激酶抑製劑PD98059(100μmol/L)和PI3K激酶抑製劑wortmannin(100nmol/L)阻斷。結論實驗結果錶明腎素前體誘導血管平滑肌細胞產生的增殖是通過ERK1/2和Akt通路髮揮作用。
목적탐토신소전체(prorenin)유도대서혈관평활기세포적증식시부통과ERK1/2화Akt통로。방법이용[3H]동위소표기적흉감적결합검측혈관평활기세포증식。단백인기분석검측신소전체유도적평활기세포ERK화Akt적활화。결과신소전체제량의뢰성유도ERK화Akt린산화,재20min체도고봉。20nmol/L신소전체처리세포48h후세포내[3H]동위소표기적흉감함량증다(P<0.05),저충촉진세포증식적작용가이피예처리ERK격매억제제PD98059(100μmol/L)화PI3K격매억제제wortmannin(100nmol/L)조단。결론실험결과표명신소전체유도혈관평활기세포산생적증식시통과ERK1/2화Akt통로발휘작용。
Objective To investigate the effect of prorenin on vascular smooth muscle cell(VSMC) proliferation via ERK and Akt activation dependent pathway.Methods DNA synthesis in rat VSMCs was measuring by [3H] thymidine.Extracellular signal-regulated kinase(ERK) and Akt phosphorylation were measured by Western blotting.Results Rat recombinant prorenin dose-dependently induced ERK and Akt phosphorylation with a peak at 20min. Prorenin(20nmol/L,48h) significantly increase VSMC [3H] thymidine incorporation,which attenuated by pretreatment with ERK kinase inhibitor,PD98059(100μmol/L),and PI3 kinase inhibitors,wortmannin(100nmol/L).Conclusion ERK and Akt activation contributes to prorenin-induced proliferative effects in VSMCs.