Regulation of Kruppel-like factor 2 (KLF2) in the pathogenesis of intracranial aneurysm induced by hemodynamics

Kruppel-like factor 2 (KLF2) has been found to regulate the reconstruction of vascular wall tissue and participate in the pathogenic mechanism of intracranial aneurysms. However, there is a paucity of research in this area. The present study aimed to investigate the regulatory effect of KLF2 on intracranial aneurysm (IA) and explore novel therapeutic strategies for treating IA. Experimental animal models were established with SPF New Zealand rabbits by bilateral carotid artery ligation (BCAL). Morphology of basilar artery bifurcation was detected using HE, EVG, Masson and immunohistochemical (IHC) staining. Vascular smooth muscle cells were harvested from basilar artery and cultured to establish KLF2 up-regulated and down-regulated cell models. The mRNA expression of KLF2, eNOS, ICAM-1 and MMP-9 were detected using real-time quantitate PCR (RT-qPCR). Protein expression of KLF2 and MAPKs pathway were measured using western blot. IA models were successfully established by bilateral carotid artery ligation. KLF2 expression was inconsistent with the variation of hemodynamics. In the KLF2 overexpression group, the mRNA expression of eNOS was increased, while that of ICAM-1 and MMP-9 was decreased. When KLF2 was up-regulated, the phosphorylation activity of p38 pathway was increased. In conclusion, results reveal that KLF2 is up-regulated in the vascular wall of basilar artery, and its overexpression regulates the pathogenesis of IA, which may be a self-protection mechanism of the arterial wall, providing a novel insight for therapy of IA.