王璨 陶輝 蔣書美 王立超 石開虎
摘?要:目的:探究微小RNA146a(miR146a)與趨化因子受體4(CXCR4)在糖尿病心肌病心肌成纖維細(xì)胞(CFs)中的表達(dá)變化。方法:提取原代心肌成纖維細(xì)胞(Cardiac?fibroblasts,CFs),高糖(33.3mmol·L1)作用CFs。用qRTPCR檢測CFs中miR146a的表達(dá),Western?blotting檢測CFs中α平滑肌肌動蛋白(αSMA)、Ⅰ型膠原前膠原A1(Col1A1)、CXCR4蛋白的表達(dá)情況。MTT檢測高糖對CFs增殖活性的影響。結(jié)果:與正常對照組相比,高糖誘導(dǎo)后的CFs中miR146a表達(dá)量降低,而高糖誘導(dǎo)后的CFs中αSMA、Col1A1、CXCR4表達(dá)增加。并且高糖處理后CFs增殖活性提高。結(jié)論:糖尿病心肌病形成過程中CFs中miR146a表達(dá)下調(diào),而CXCR4表達(dá)上調(diào),提示miR146a與CXCR4糖尿病心肌病的病程中可能存在潛在的調(diào)節(jié)關(guān)系,有助于探索糖尿病心肌病的病理機(jī)制。
關(guān)鍵詞:miR146a;CXCR4;糖尿病心肌病;心肌纖維化
中圖分類號:R?542.23
To?investigate?the?expression?changes?ofMicroRNA146a?and?CXCR4
in?myocardial?tissue?and?fibroblasts?of?diabetic?cardiomyopathy
Wang?Can1,2?Tao?Hui1,2?Jiang?Shumei1,2?Wang?Lichao1,2?Shi?Kaihu1,2*
1.Dept?of?Cardiothoracic?Surgery,The?Second?Affiliated?Hospital?of?Anhui?Medical?University?AnhuiHefei?230601;
2.Cardiovascular?Research?Center,Anhui?Medical?University?AnhuiHefei?230601
Abstract:Objective:To?investigate?the?expression?changes?of?microRNA146a?(miR146a)?and?chemokine?receptor?4?(CXCR4)?in?diabetic?cardiomyopathy?myocardial?fibroblasts?(CFS).Methods:CFS?were?extracted?and?high?glucose?(33.3mmol·L1)?was?used?to?induce?CFs.Use?qRTPCR?in?the?detection?of?CFs?miR146a?express,Western?blotting?detection?in?CFs?the?expression?of?αSMA,Col1A1,and?CXCR4.MTT?was?used?to?detect?the?effect?of?high?glucose?on?the?proliferation?of?CFS.Results:Compared?with?the?normal?control?group,the?expression?of?miR146a?decreased?in?CFs?induced?by?high?glucose,while?the?expression?of?αSMA,Col1A1?and?CXCR4?increased?in?CFs?induced?by?high?glucose.The?proliferation?activity?of?CFs?was?increased?after?high?glucose?treatment.Conclusion:During?the?formation?of?diabetic?cardiomyopathy,miR146a?expression?is?downregulated?in?CFs,while?CXCR4?expression?is?upregulated,suggesting?that?there?may?be?a?potential?regulatory?relationship?between?miR146a?and?CXCR4?in?the?course?of?diabetic?cardiomyopathy,which?is?helpful?to?explore?the?pathological?mechanism?of?diabetic?cardiomyopathy.