MIRNA-29B PARTICIPATES IN THE DEVELOPMENT OF INTRACRANIAL ANEURYSMS BY MEDIATING THE TARGET GENE BECLIN1 TO REGULATE SMOOTH MUSCLE CELL AUTOPHAGY

Ying Cui, Dawei Wang, Qing Chao, Qiujian Zhang, Hao Wang^* 

Department of Neurosurgery, The 2nd Affiliated Hospital of Bengbu Medical College, Bengbu, PR China

Objective: To explore the mechanism by which microRNA-29b (miRNA-29b) is involved in the occurrence of intracranial aneurysms via mediation of the target gene Beclin1 to regulate smooth muscle cell autophagy.

Methods: The 22 human intracranial aneurysm tissues included in this study were all taken from patients with intracranial aneurysms admitted to our hospital between January 2013 and May 2015. The 22 normal cerebral artery tissues were collected from brain tumor patients who underwent craniotomy at our hospital during the same period. We collected 42 SPF rats and randomly selected 21 intracranial aneurysm rat models; the remaining 21 rats were left untreated, and their normal cerebral artery tissues were taken. The relative expression levels of miRNA-29b in human and rat intracranial aneurysm tissues and normal cerebral artery tissues were compared. Human aortic smooth muscle cells were cultured and randomly divided into a negative control group (transfected with miRNA-29b mimics NC) and a miRNA-29b group (transfected with miRNA-29b mimics). Twenty-four hours after transfection, some cells in the miRNA-29b group were treated with 20 mg/L ox-LDL, while the negative control group was not treated. At 48 hours after transfection of the remaining cells, the miRNA-29b, Beclin1 and Beclin1, and LC3II/I protein expression levels of the two groups of cells were compared. The cell proliferation rates of the two groups were further analyzed.

Results: The relative expression level of miRNA-29b in human intracranial aneurysm tissue was significantly lower than that in normal brain arteries (p<0.01). The relative expression level of miRNA-29b in rat intracranial aneurysm tissue was significantly lower than that in normal cerebral artery tissue (p<0.01). After ox-LDL intervention, the relative expression of miRNA-29b in smooth muscle cells of miRNA-29b group was significantly lower than that of the negative control group (p<0.01). After 48h post-transfection, the relative expression and protein expression of Beclin1 in smooth muscle cells from the miRNA-29b group were significantly lower than those of the negative control group, while the expression of the LC3II/I protein was significantly higher than in the control group (p<0.01). At 48 hours after transfection, the proliferation capacity of smooth muscle cells in the miRNA-29b group was significantly lower than that in the control group (p<0.01). 

Conclusion: miRNA-29b can participate in the occurrence of intracranial aneurysms by mediating the target gene Beclin1 to regulate smooth muscle cell autophagy.