Lu Mei-Hua, Chao Chung-Faye, Huang Chung-Guei, Chang Li-Tze
Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan, ROC.
Clin Exp Hypertens. 2003 Oct;25(7):413-25. doi: 10.1081/ceh-120024985.
The effect of endothelium-released vasoactive factors on vascular smooth muscle cell (VSMC) proliferation was studied in a coculture system. Isolated aortic endothelial cells and smooth muscle cells from 4-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats were cocultured. After coculture, the VSMC proliferation rate was examined by 3H-thymidine incorporation assay and the levels of the vasoactive factors in medium were determined by enzyme immunoassay (EIA). The results indicate that the proliferation rate of VSMCs in SHR was significantly higher than in WKY rats when VSMCs were cultured alone. When SHR vascular endothelial cells (VECs) were cocultured with VSMCs, the proliferation rate of SHR VSMCs was enhanced; however, there was no growth promoting effect in WKY VSMCs. When WKY VECs were cocultured with VSMCs, no VSMC proliferation effect was observed. When VSMCs were cultured alone, the endothelin-1 (ET-1) secretion in SHR was significantly higher than in WKY rats. When VECs and VSMCs were cocultured, the ET-1 concentration increased in both SHR VEC and WKY VEC coculture groups in a similar manner; but the SHR VECs tended to release more thromboxaneA2 (TXA2) and less PGI2 than WKY VECs. These results suggest that some kind of interaction between SHR VSMCs and SHR VECs is responsible for the high proliferation of SHR VSMCs but not the effects of SHR VECs per se.
在共培养系统中研究了内皮释放的血管活性因子对血管平滑肌细胞（VSMC）增殖的影响。将4周龄自发性高血压大鼠（SHR）和年龄匹配的Wistar-Kyoto（WKY）大鼠分离的主动脉内皮细胞和平滑肌细胞进行共培养。共培养后，通过3H-胸腺嘧啶核苷掺入试验检测VSMC增殖率，并通过酶免疫测定（EIA）测定培养基中血管活性因子的水平。结果表明，单独培养时，SHR中VSMC的增殖率显著高于WKY大鼠。当SHR血管内皮细胞（VEC）与VSMC共培养时，SHR VSMC的增殖率增强；然而，WKY VSMC没有生长促进作用。当WKY VEC与VSMC共培养时，未观察到VSMC增殖效应。单独培养VSMC时，SHR中内皮素-1（ET-1）的分泌显著高于WKY大鼠。当VEC和VSMC共培养时，SHR VEC和WKY VEC共培养组中ET-1浓度以相似的方式增加；但与WKY VEC相比，SHR VEC倾向于释放更多的血栓素A2（TXA2）和更少的前列环素（PGI2）。这些结果表明，SHR VSMC和SHR VEC之间的某种相互作用是SHR VSMC高增殖的原因，而不是SHR VEC本身的作用。
