Abstract
Intracranial aneurysm (IA) is a common cerebrovascular disease. Understanding the mechanism regulating the progression of IA could help to develop novel therapeutic methods for this disease. In this study, we confirmed FGB is one of the targets of miR-139-5p. Moreover, miR-139-5p expression in intracranial aneurysm specimens was suppressed compared with normal tissues. However, we found that FGB in intracranial aneurysm samples was remarkedly enhanced compared to normal tissues. Moreover, we found miR-139-5p overexpression and FGB silencing inhibit HBMEC proliferation and tube formation and suppressed α-SMA and CXCR4 levels in HBMEC cells. Furthermore, a rescue experiment confirmed miR-139-5p affected the proliferation and angiogenesis of HBMEC through FGB. Despite further research being needed to determine the exact functions of miR-139-5p in the formation of CA, our new findings contribute to a comprehensive understanding of the treatment mechanism of IA.