CGRP对ET-1诱导的大鼠血管平滑肌细胞表型转化和增殖的影响  被引量:1

Effects of CGRP on ET-1-induced phenotype and proliferation of vascular smooth muscle cells in rats

在线阅读下载全文

作  者:徐红涛[1] 李玉华[1] 王旻晨[2] 王晓春[2] 吴芹[1] 马林伟[1] 

机构地区:[1]盐城卫生职业技术学院,江苏省224006 [2]苏州大学医学院解剖系

出  处:《江苏医药》2015年第13期1499-1501,F0003,共4页Jiangsu Medical Journal

基  金:盐城市医学科技发展项目(YK2102030)

摘  要:目的探讨降钙素基因相关肽(CGRP)对内皮素1(ET-1)诱导的大鼠血管平滑肌细胞(VSMCs)表型转化和增殖的作用及其可能机制。方法将原代培养的VSMCs分为对照组(A组)、ET-1组(B组)、ET-1+CGRP组(C组,ET-1预处理24h后共培养24h)和CGRP+ET-1组(D组,CGRP预处理24h后共培养24h)。采用免疫细胞化学染色检测细胞增殖,RT-PCR检测高血压相关基因1(HRG-1)和平滑肌22α(SM22α)mRNA表达。结果与A组相比,B组细胞增殖增加,HRG-1和SM22αmRNA表达下调(P<0.05);而与B、C组相比,D组细胞增殖减少,HRG-1和SM22αmRNA表达上调(P<0.05)。结论 CGRP预处理能明显抑制ET-1诱导的VSMCs表型转化和增殖,可能与HRG-1和SM22α表达上调有关。Objective To investigate the effect and underlying mechanism of calcitonin generelated peptide(CGRP)on the endothelin 1(ET-1)-induced phenotype and proliferation of vascular smooth muscle cells(VSMCs)in rats.Methods VSMCs were primarily cultured in vitro and divided into four groups of A(normal control),B(treated with ET-1),C(pretreated with ET-1for 24 hours and followed by ET-1plus CGRP for 24hours)and D(pretreated with CGRP for 24 hours and followed by CGRP plus ET-1for 24hours).Cell proliferation was determined by immunocytochemical staining,and mRNA expressions of hypertension related gene-1(HRG-1)and smooth muscle 22alpha(SM22α)were detected by RT-PCR.Results Compared with group A,cell proliferation was increased,but mRNA expressions of HRG-1and SM22αwere downregulated in group B(P〈0.05).However,compared with groups of B and C,cell proliferation was decreased,but mRNA expressions of HRG-1and SM22αwere upregulated in group D(P〈0.05).Conclusion CGRP pretreatment can significantly inhibit ET-1-induced phenotype and proliferation of VSMCs,which may be related to the upregulation of HRG-1and SM22αexpressions.

关 键 词:降钙素基因相关肽 内皮素1 血管平滑肌细胞 

分 类 号:R363[医药卫生—病理学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象