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目的:探讨血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)对骨髓间充质干细胞(mesenchymal stem cells,MSCs)中信号转导和转录激活因子3(signal transducer and activator of transcription 3,STAT3)水平的调节,分析STAT3在AngⅡ诱导MSCs的血管内皮生长因子(vascular endothelial growth factor,VEGF)表达增加中的作用,研究血管紧张素转化酶(angiotensin convertingenzyme,ACE)与AngⅡ刺激诱导的STAT3磷酸化之间的关系。方法:分离培养大鼠MSCs,以AngⅡ处理细胞,并用针对STAT3的小干扰RNA(STAT3 siRNA)或ACE抑制剂卡多普利提前进行干预。用免疫印迹法(Western blot)检测细胞内STAT3磷酸化和ACE表达水平;用Real-time PCR法检测细胞内VEGF mRNA表达水平;用ELISA法检测培养液中VEGF蛋白水平。结果:①在MSCs中,AngⅡ诱导STAT3的磷酸化水平增加;②STAT3 siRNA明显抑制AngⅡ诱导的VEGF表达和分泌;③卡托普利显著抑制了AngⅡ诱导的STAT3磷酸化。结论:在MSCs中,STAT3参与了AngⅡ诱导的VEGF表达,并且AngⅡ诱导的STAT3具有ACE依赖性。
AIM: To investigate the regulation of signal transducer and activator of transcription 3 (STAT3) levels by angiotensin Ⅱ (AngⅡ) in mesenchymal stem cells (MSCs) To study the role of STAT3 in the induction of vascular endothelial growth factor (VEGF) expression induced by Ang II in MSCs, and to investigate the relationship between angiotensin-converting enzyme (ACE) and STAT3 phosphorylation induced by AngⅡ. METHODS: Rat MSCs were isolated and cultured. AngⅡ-treated cells were treated with STAT3 siRNA or STAT inhibitor ACE inhibitor Cardopril. The levels of STAT3 phosphorylation and ACE were detected by Western blot. The expression of VEGF mRNA was detected by Real-time PCR. The VEGF protein level was detected by ELISA. RESULTS: ①In MSCs, the level of phosphorylation of STAT3 was increased by AngⅡ; ②STAT3 siRNA significantly inhibited AngⅡ-induced VEGF expression and secretion; ③ Captopril significantly inhibited the phosphorylation of STAT3 induced by AngⅡ. Conclusion: In MSCs, STAT3 is involved in Ang Ⅱ-induced VEGF expression, and AngⅡ-induced STAT3 is ACE-dependent.