细菌性颅内动脉瘤72-和92-KDa IV型胶原酶及其组织抑制因子mRNA的原位杂交  

In situ localization of mRNA for 72-and 92-KDa type IV collagenase and their tissue inhibitors in bacterial intracranial aneurysms

作　　者：韩利江[1] 赵继宗[1] 孙异临[1] 张东[1] 

机构地区：[1]北京天坛医院神经外科,100050

出　　处：《中华实验外科杂志》2000年第2期145-146,共2页Chinese Journal of Experimental Surgery

基　　金：国家自然科学基金! ( 3 9670 73 7)

摘　　要：目的　探讨细菌性颅内动脉瘤 (BIAs)的发病机理。方法　用地高辛标记的 72 和92 KDaIV型胶原酶 (MMP 2和MMP 9)及其组织抑制因子 (TIMP) 1、TIMP 2反义RNA探针与BIAs(n =2 )和正常脑动脉组织 (n =6 )进行原位杂交 ,定位产生它们的细胞。并用正义RNA探针进行阴性对照。结果　 2份感染性颅内动脉瘤标本中均见MMP 9mRNA阳性杂交信号。且在内膜 ,尤其是相当于内弹力层部位 ,阳性杂交信号密集存在。动脉瘤壁内弹力层消失。阳性杂交信号定位于单核细胞、成纤维细胞和平滑肌细胞。正常脑动脉标本中未发现MMP 9mRNA阳性杂交信号。在BIAs和正常脑动脉组织中未发现MMP 2、TIMP 1和TIMP 2的mRNA阳性杂交信号。结论　感染因素引起炎性细胞浸润 ,表达MMP 9mRNA增多 ,导致内弹力层断裂、消失 ,甚至动脉壁全层结构的破坏 ,从而引发BIAs形成。Objective\ To study the pathogenesis of bacterial intracranial aneurysms (BIAs). Methods\ In situ hybridization of RNA probes of 72 or 92 Kda type IV collagenase (MMP 2, MMP 9) and tissue inhibiting factors (TIMP) 1,TIMP 2 labeled with digoxingenin with histologic sections of BIAs ( n =2) or normal ( n =6) cerebral arteries was performed respectively to localize the cells producing MMP 2, MMP 9 and TIMP 1. The sense RNA probes served as negative control. Results\ The levels of MMP 9 mRNAs were very high in BIAs, especially in the site of internal elastic lamella. But none of MMP 9 mRNA was found in normal cerebral arteries. None of MMP 2, TIMP 1 or TIMP 2 mRNA existed in either BIAs or normal cerebral arteries. In situ studies localized tissue MMP 9 expression on monocytes, fibroblasts, smooth muscle cells in aneurysmal wall. Conclusion\ Differential patterns of expression seen in situ and elevated tissue MMP 9 mRNA levels in bacterial aneurysm versus normal cerebral artery suggest that high level of MMP 9 due to monocyte might be responsible for the destruction of internal elastic lamina or even all laminae of cerebral arteries which lead to BIAs.

关 键 词：颅内动脉瘤 细菌性 原位杂交 胶原酶 MRNA 

分 类 号：R741.02[医药卫生—神经病学与精神病学]