摘要
目的观察移植后心脏组织中热休克蛋白27（HSP27）和糖调节蛋白78（GRP78）的组织分布，探讨移植后心脏血管病变（CAV）的发病机制。方法建立大鼠同基因（n=8）和异基因（n=8）心脏移植的Ono模型，采用免疫组织化学法[链霉菌抗生物素蛋白-过氧化物酶（sP）法]验证移植后心脏组织中HSP27和GRP78的组织分布。结果同基因植组，HSP27和GRP78在心脏组织内均匀分布；异基因移植组，HSP27和GRP78在环血管周围心肌组织中高表达（2．24±0．36比1．04±0．10，P〈0．01；1．51±0．12比0．85±0．30，P〈0．05），而在增生的冠状动脉组织内几乎不表达（2．24±0．36比0．25±0．08，P〈0．01；1．51±0．12比0．16±0．10，P〈0．01）。结论HSP27和GRP78在异基因移植后心脏组织中分布不均，导致冠状动脉组织无力对抗免疫损伤，诱发血管平滑肌细胞过度增殖可能是CAV发生、发展的重要原因。
Objective -To-observe the protein expression of heat shock protein 27 （HSP27） and glucose regulated protein 78 （GRP78） in rats transplanted hearts, and provide some clues to elucidate the pathogenesis of cardiac allograft vasculopathy （CAV）. Methods The hearts were transplanted from Lewis to Sprague-Dawely rats as allograft （ n = 8 ） and from Lewis to Lewis rats as isograft （ n = 8 ） based on Ono＇ s model. The protein expression of HSP27 and GRP78 was detected by using immunohistochemistry [ streptavid-inperoxidase （SP） method ]. Results The expression of HSP27 and GRP78 was stained uni- fomrly in cardiac isografts, but that was anomalous in cardiac allografts, which showed higher expression on cardiac muscle （2. 24 ± 0. 36 vs. 1.04 ± 0. 10, P 〈 0.01 ;1. 51 ±0. 12 vs.0. 85 ±0. 30, P 〈 0. 05 ） and lower expression on blood vessels in biopsies with CAV （2. 24 ± 0. 36 vs. 0. 25 ± 0. 08, P 〈 0. 01 ; 1.51± 0. 12 vs. 0. 16 ±0. 10,P 〈 0. 01 ）. Conclusion The less expression of HSP27 and GRP78 on blood vessels decreased the defense to immunologic injury, which stimulated the over-proliferation of vascular smooth muscle cells to repair the vessels damage in heart allografts. Meanwhile, these protective reactions could incur the de- velopment of CAV in heart allografts.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2013年第8期1571-1573,共3页
Chinese Journal of Experimental Surgery
基金
安徽医科大学校科学研究基金资助项目（2010xkj088）
关键词
心脏移植
血管病变
热休克蛋白27
糖调节蛋白78
Cardiac allograft
Vasculopathy
Heat shock protein 27
Glucose regulated protein 78
