Schelling P, Ganten D, Speck G, Fischer H
J Cell Physiol. 1979 Mar;98(3):503-13. doi: 10.1002/jcp.1040980309.
Components of the renin-angiotensin system were studied in established cell culture lines of 3T3 and SV3T3 mouse fibroblasts. The renin content in 3T3 cells was significantly higher than in virus-transformed SV3T3 cells. With time after infection, renin decreased in Simian virus 40 transformed cells, while it increased steadily in mock-infected 3T3 cells. In contrast to renin, angiotensinase activity was higher in SV3T3 cells. Angiotensin II stimulated cell proliferation in 3T3 mouse fibroblasts and decreased their renin content in a dose-related manner. In contrast, saralasin, an angiotensin receptor antagonist, inhibited cell growth in 3T3 and SV3T3 cells and caused an increase of cellular renin concentration. The angiotensin fragments angiotensin (2-8) heptapeptide and angiotensin (4-8) pentapeptide had no effect on cell growth. A significant negative correlation was found between cell proliferation and renin levels in 3T3 and SV3T3 cells irrespective of the treatment. Our results indicate (1) that angiotensin II may be involved in cell growth regulation, (2) that a negative feedback exist between angiotensin II added and intracellular renin content, and (3) that virus infection causes a decrease in intracellular renin synthesis, while non-specific angiotensinase activity is increased under this condition.
在3T3和SV3T3小鼠成纤维细胞的既定细胞系中研究了肾素 - 血管紧张素系统的组成部分。3T3细胞中的肾素含量显著高于病毒转化的SV3T3细胞。感染后随着时间的推移，猿猴病毒40转化细胞中的肾素减少，而在模拟感染的3T3细胞中肾素稳步增加。与肾素相反，血管紧张素酶活性在SV3T3细胞中更高。血管紧张素II刺激3T3小鼠成纤维细胞的细胞增殖，并以剂量相关的方式降低其肾素含量。相比之下，血管紧张素受体拮抗剂沙拉新抑制3T3和SV3T3细胞的细胞生长，并导致细胞肾素浓度增加。血管紧张素片段血管紧张素（2 - 8）七肽和血管紧张素（4 - 8）五肽对细胞生长没有影响。无论处理如何，在3T3和SV3T3细胞中均发现细胞增殖与肾素水平之间存在显著的负相关。我们的结果表明：（1）血管紧张素II可能参与细胞生长调节；（2）添加的血管紧张素II与细胞内肾素含量之间存在负反馈；（3）病毒感染导致细胞内肾素合成减少，而在此条件下非特异性血管紧张素酶活性增加。
