LncRNA Xist induces arterial smooth muscle cell apoptosis in thoracic aortic aneurysm through miR-29b-3p/Eln pathway.

Background: Thoracic aortic aneurysm (TAA) is a serious disease usually happening in elder people and with high death rate. Accumulating studies have reported that long non-coding RNAs (lncRNAs) are implicated in the progression of various human diseases, including TAA.

Aim: In our study, we intended to explore the function of elastin (Eln) and its upstream mechanism in TAA.

Methods: RT-qPCR determined gene expressions and western blot tested changes in protein levels. Ang Ⅱ treatment was implemented to induce cell apoptosis. Flow cytometry analysis, TUNEL assay and JC-1 assay were exploited to measure cell apoptosis. Meanwhile, mechanistic assays such as RIP, RNA pull down and luciferase reporter assays were employed to identify the interplay between RNAs.

Results: Eln inhibition was identified to protect rat arterial smooth muscle cells from apoptosis. Also, miR-29b-3p was identified to bind to Eln, and X inactive specific transcript (Xist) could boost Eln expression through absorbing miR-29b-3p. Meanwhile, Eln overexpression counteracted the suppression of silenced Xist on the apoptosis of rat arterial smooth muscle cells. More importantly, such ceRNA network was proved to aggravate the apoptosis of human aortic smooth muscle cells.

Conclusion: LncRNA Xist contributes to arterial smooth muscle cell apoptosis through miR-29b-3p/Eln pathway, providing new potential roads for treating TAA.