# LncRNA HCG18 affects aortic dissection through the miR-103a-3p/HMGA2 axis by modulating proliferation and apoptosis of vascular smoothing muscle cells

## TL;DR

This study shows that the lncRNA HCG18 contributes to aortic dissection by affecting vascular smooth muscle cell behavior through a specific molecular pathway.

## Contribution

The study identifies a novel regulatory axis involving HCG18, miR-103a-3p, and HMGA2 in aortic dissection.

## Key findings

- HCG18 and HMGA2 are upregulated in aortic tissues of AD patients.
- Downregulating HCG18 enhances VSMC proliferation and reduces apoptosis.
- HCG18 promotes HMGA2 expression by competing with miR-103a-3p.

## Abstract

Image, graphical abstract

•Downregulating HCG18 enhances VSMC proliferation and reduces apoptosis.•HCG18/miR-103a-3p/HMGA2 axis affects VSMC proliferation and apoptosis.•Downregulating HCG18 improves the pathological injury of the aorta in AD rats.

Downregulating HCG18 enhances VSMC proliferation and reduces apoptosis.

HCG18/miR-103a-3p/HMGA2 axis affects VSMC proliferation and apoptosis.

Downregulating HCG18 improves the pathological injury of the aorta in AD rats.

Aortic Dissection (AD) is a vascular disease with a high mortality rate and limited treatment strategies. The current research analyzed the function and regulatory mechanism of lncRNA HCG18 in AD.

HCG18, miR-103a-3p, and HMGA2 levels in the aortic tissue of AD patients were examined by RT-qPCR. After transfection with relevant plasmids, the proliferation of rat aortic Vascular Smoothing Muscle Cells (VSMCs) was detected by CCK-8 and colony formation assay, Bcl-2 and Bax was measured by Western blot, and apoptosis was checked by flow cytometry. Then, the targeting relationship between miR-103a-3p and HCG18 or HMGA2 was verified by bioinformation website analysis and dual luciferase reporter assay. Finally, the effect of HCG18 was verified in an AD rat model induced by β-aminopropionitrile.

HCG18 and HMGA2 were upregulated and miR-103a-3p was downregulated in the aortic tissues of AD patients. Downregulating HCG18 or upregulating miR-103a-3p enhanced the proliferation of VSMCs and limited cell apoptosis. HCG18 promoted HMGA2 expression by competing with miR-103a-3p and restoring HMGA2 could impair the effect of HCG18 downregulation or miR-103a-3p upregulation in mediating the proliferation and apoptosis of VSMCs. In addition, down-regulation of HCG18 could improve the pathological injury of the aorta in AD rats.

HCG18 reduces proliferation and induces apoptosis of VSMCs through the miR-103a-3p/HMGA2 axis, thus aggravating AD.