LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm

Background: MiR-130a is a recently identified critical player in vascular smooth muscle cell (VSMC) proliferation, which participates in intracranial aneurysm (IA). However, the involvement of miR-130a in IA and its upstream regulator are unknown. Our preliminary sequencing analysis revealed a close correlation between miR-130a and lncRNA SAMMSON across IA samples. Therefore, we further studied the crosstalk between SAMMSON and miR-130a in IA. Methods: SAMMSON and miR-130a expression were measured using RT-qPCR. SAMMSON subcellular location was analyzed with nuclear fractionation assay. Their direct interaction was explored with RNA pull-down assay. The role of SAMMSON in miR-130a maturation was studied with overexpression analysis. VSMC cell proliferation was analyzed with BrdU assay. Results: SAMMSON and premature miR-130a were deregulated in IA, while mature miR130a was upregulated in IA. SAMMSON is localized in both the nucleus and cytoplasm, and direct interaction between SAMMSON and miR-130a was observed. SAMMSON over expression suppressed miR-130a maturation in VSMCs and reduced the enhancing effects of miR-130a on VSMC cell proliferation. Conclusion: SAMMSON is overexpressed in IA and suppresses VSMC proliferation via inhibiting miR-130a maturation.

Automated summary

The study revealed that SAMMSON is overexpressed in intracranial aneurysm (IA) and suppresses vascular smooth muscle cell (VSMC) proliferation by inhibiting the maturation of miR-130a.