Shyu K G, Chen J J, Shih N L, Chang H, Wang D L, Lien W P, Liew C C
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, R.O.C.
Biochem Biophys Res Commun. 1995 Jun 6;211(1):241-8. doi: 10.1006/bbrc.1995.1802.
The effect of cyclical mechanical stretch on angiotensinogen gene expression was examined using a neonatal rat cardiocyte culture system. Cultured cardiocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation, at 60 cycles/min. The angiotensinogen gene was activated 2 to 5 fold after stretch for 3 to 24 hr, as shown by quantitative reverse transcription polymerase chain reaction. The 5'-flanking region of the angiotensinogen promoter was activated after stretch for 24 hr. This gene expression could be completely suppressed by losartan, a specific antagonist of angiotensin II receptor. These results indicate that (1) cyclical mechanical stretching of cardiocytes is a good model for the study of cardiac hypertrophy-related gene expression; (2) cyclical stretch up-regulates expression of the angiotensinogen gene and (3) the increase in promoter activity may contribute to the induction of angiotensinogen mRNA by cyclical stretch.
使用新生大鼠心肌细胞培养系统研究了周期性机械拉伸对血管紧张素原基因表达的影响。在柔性膜基质上生长的培养心肌细胞通过真空拉伸至最大伸长率的20%，频率为每分钟60次循环。定量逆转录聚合酶链反应显示，拉伸3至24小时后，血管紧张素原基因被激活2至5倍。拉伸24小时后，血管紧张素原启动子的5'侧翼区域被激活。这种基因表达可被血管紧张素II受体特异性拮抗剂氯沙坦完全抑制。这些结果表明：（1）心肌细胞的周期性机械拉伸是研究心脏肥大相关基因表达的良好模型；（2）周期性拉伸上调血管紧张素原基因的表达；（3）启动子活性的增加可能有助于周期性拉伸诱导血管紧张素原mRNA。
