摘要
目的研究血管紧张素Ⅱ致心肌细胞肥大过程中组蛋白脱乙酰基酶2的表达。方法培养原代心肌细胞,给予不同浓度的血管紧张素Ⅱ刺激心肌细胞造成肥大,取心肌细胞进行逆转录聚合酶链反应观察组蛋白脱乙酰基酶2和β-肌球蛋白重链mRNA表达,免疫组织化学法检测组蛋白脱乙酰基酶2和c-fos蛋白表达,相差显微镜观察细胞面积变化。结果经血管紧张素Ⅱ刺激后在相差显微镜下可见心肌细胞面积变大,而且随着血管紧张素Ⅱ浓度的增加而增大。组蛋白脱乙酰基酶2和β-肌球蛋白重链mRNA水平及组蛋白脱乙酰基酶2和c-fos蛋白表达随着血管紧张素Ⅱ浓度的增加而增加。结论血管紧张素Ⅱ致心肌细胞肥大过程中伴有组蛋白脱乙酰基酶2表达增加,后者有可能参与心肌细胞的肥大机制。
Aim To observe the expression of histone deacetylase 2 (HDAC 2) in hypertrophic cardiocytes induced by angiotensin Ⅱ ( Ang Ⅱ ). Methods The cultured cardiocytes were treated with Ang Ⅱ of different concentrations to induce hypertrophy. The mRNA levels of HDAC 2 and G-myosin heavy chain( β-MHC ) were exmained by reverse transcription-polymerasc chain reaction. The protein expressions of HDAC 2 and c-fos were exmanined by immuno- histochemistry method. The morphologic changes of cardiocytes were observed under the contrast phase microscope. Results Myocytes were cultured successfully. After stimulated by Ang Ⅱ the myocytes were enlarged under the contrast phase microscope. With the increasing of Ang Ⅱ concentrations (2×10^-6 mol/L, 2×10^-7 mol/L and 2×10^-8 mol/L) , the mRNA levels of HDAC 2 and IB-MHC increased. The immunohistocbemistry results showed that the protein expressions of HDAC 2 and c-fos also increased in the hypertrophic cardiocytes. The areas of the myocytes increased with different Ang Ⅱ(P 〈 0.05 ). Conclusions The expression of HDAC 2 increased in hypertrophic cardiocytes stimulated by AngⅡ. HDAC 2 may play a role in cardiocyte hypertrophy.
出处
《中国动脉硬化杂志》
CAS
CSCD
北大核心
2009年第5期367-370,共4页
Chinese Journal of Arteriosclerosis
基金
黑龙江省卫生厅课题(2005-295)