脑血管畸形血管自动调节功能异常的分子机制探讨

The Molecular Mechanism of Dysautoregulation of Malformed Cerebral Vessels

目的 探讨脑血管畸形(AVMs)血管自动调节功能异常的分子机制。方法 14例AVMs及周边脑组织行显微外科手术切除,标本提取总RNA,应用RT-PCR检测脑AVMs中ppET-l和ET_A表达变化,并与8例正常脑血管标本进行比较。结果 在脑血管畸形血管中,发现ppET-lmRNA和ET_AmRNA表达较正常脑血管下降。结论 脑AVMs中ppET-lmRNA表达的下降可能会导致AVMs中ET-l的下降,而脑AVMs中ET-1下降很可能是畸形血管自动调节功能异常的主要原因之一;ET_AmRNA表达较正常脑血管下降,可能阻止外源性ET-l,并加强脑AVMs中ET-l的抑制作用,导致脑AVMs血管自动调节功能异常。

Objective To explore the molecular mechanism of dysautoregulation of malformed cerebral vessels. Methods Total RNA was abstracted from 14 samples of arteriovenous malformations , and adjacent brain tissues and 8 normal cerebral vessels which were removed by microneurosurgery. The expressions of ppET - 1 and ETA receptor in AVMs were detected by RT - PCR. Results The expressions of ppET - 1 and ETA receptor mRNA in AVMs were lower than these in normal cerebral vessels. Conclusion Downregulation of expressions of ppET - 1 mRNA contributed to the lack of ET - 1 secretion in AVMs. Downregulation of ET - 1 has been implicated in a variety of vascular disorders involving both he-modynamic and structural changes in the vasculture. The decrease of ETA mRNA expression on AVM would prevent gene repression from exogenous sources of ET - 1 and reinforce the biological consequences of ET - 1 in AVMs,thus resulting in dysautoregulation of cerebral vessels in AVMs.