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机构地区:[1]华中科技大学同济医学院附属协和医院心血管外科,武汉430022
出 处:《中华实验外科杂志》2011年第10期1756-1757,I0003,共3页Chinese Journal of Experimental Surgery
基 金:国家自然科学基金资助项目(C30600608、C30872540);国家“863”新材料技术资助项目(2009AA032420)
摘 要:目的探讨风湿性和退行性瓣膜钙化可能机制。方法分为风湿性病变、退行性病变(n=10)和对照组,行瓣膜钙化检测。结果苏木素.伊红(HE)染色观察病理变化,VonKossa染色显示病变瓣膜肉眼大致正常的组织内存在点状钙质沉积。免疫组织化学显示两组病变瓣膜内层见骨钙素分布,瓣膜间质细胞内见Runx2分布。逆转录.聚合酶链反应(RT-PCR)显示病变瓣膜均有Runx2(灰度值0.297±0.154和0.287±0.172)和骨钙素(灰度值0.178±0.087和0.190±0.095)mRNA表达,两组间差异无统计学意义(P〉0.05)。结论风湿性和退行性钙化瓣膜都存在Runx2活化及其下游成骨信号蛋白骨钙素表达。肉眼观不能准确判断早期瓣膜钙化。Objective To study mechanism for valve calcification in rheumatic and degenerative heart diseases. Methods In patients with rheumatic and degenerative diseases, We examined calcified hu- man heart valves which were replaced at surgery (n = 10 ). The control group was obtained from four removed hearts suffered from dilated eardiomyopathy. Results Von Kossa staining was used to assess the extent of mineralization and confirm the presence of calcification in both calcified groups. Immunohistochemistry verified the presentation of Runx2 in valve interstitial cells and osteocalcin in the endothecium of the valve. Reverse transcription-polymerase chain reaction (RT-PCR) revealed the increased mRNA levels of Ruin2 (0. 297 ±0. 154 vs. 0. 287 ±0. 172) and osteocalcin (0. 178 ±0. 087 vs. 190±0. 095). Conclu sion These findings support the concept that there is the similar mechanism of calcification in rheumatic and degenerative diseases. Meanwhile, Runx2 is a potential biological marker in the pathogenesis.
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