Yamaguchi M, Kumada K
Department of Surgery, Show University Fujigaoka Hospitals, Yokohama, Japan.
Am J Surg. 1998 Apr;175(4):334-6. doi: 10.1016/s0002-9610(98)00003-8.
Platelet-derived growth factor (PDGF) A chain, basic fibroblast growth factor (bFGF), and tissue-type plasminogen activator (tPA) from smooth muscle cells (SMCs) have been postulated to initiate SMC proliferation and migration in the process of intimal thickening.
In this study we tested whether trapidil, which is reported to reduce intimal thickening, would suppress mRNA increases for all or only some of these genes in human SMC.
Cultured human saphenous vein SMCs made quiescent by 72-hour incubation in 0.5% serum were stimulated with 3U/mL alpha-thrombin +/- trapidil. Changes in mRNA transcript levels were analyzed by Northern blot.
Trapidil decreased thrombin-induced mRNA levels for bFGF and appeared to decrease mRNA for PDGF-A chain, but not for tPA.
These results suggest that trapidil may reduce intimal thickening at least partly via the suppression of increased bFGF and PDGF-A chain mRNA levels in vascular SMCs.
平滑肌细胞(SMC)分泌的血小板源性生长因子(PDGF)A链、碱性成纤维细胞生长因子(bFGF)和组织型纤溶酶原激活剂(tPA)被认为在内膜增厚过程中启动SMC增殖和迁移。
在本研究中,我们测试了据报道可减少内膜增厚的曲匹地尔是否会抑制人SMC中所有或仅部分这些基因的mRNA增加。
将在0.5%血清中孵育72小时使静止的培养人隐静脉SMC用3U/mLα-凝血酶±曲匹地尔刺激。通过Northern印迹分析mRNA转录水平的变化。
曲匹地尔降低了凝血酶诱导的bFGF的mRNA水平,并且似乎降低了PDGF-A链的mRNA,但未降低tPA的mRNA。
这些结果表明,曲匹地尔可能至少部分通过抑制血管SMC中bFGF和PDGF-A链mRNA水平的增加来减少内膜增厚。