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hsa_circ_0021001 modulates human brain vascular smooth muscle cell viability in intracranial aneurysm through the
Jie Cao1, Qiujiang Xi1, Jianqing Yuan1
1Department of Neurology, The First Affiliated Hospital of Gannan Medical University Ganzhou 341000, Jiangxi, China.
Insights
Circular RNA hsa_circ_0021001 regulates intracranial aneurysm by affecting human brain vascular smooth muscle cells. It modulates Gremlin 1 expression via miR-152-3p, impacting cell viability and migration.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Intracranial aneurysm (IA) is linked to human brain vascular smooth muscle cell (hBVSMC) dysfunction.
- The role of hsa_circ_0021001 in IA pathogenesis and its mechanism in hBVSMC dysfunction are not fully understood.
Purpose of the Study:
- To investigate the mechanism by which hsa_circ_0021001 influences hBVSMC function in the context of IA.
- To elucidate the regulatory relationship between hsa_circ_0021001, miR-152-3p, and Gremlin 1 (GREM1) in hBVSMCs.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) to detect gene expression.
- Cell Counting Kit-8 (CCK-8) assays for cell viability.
- Western blotting for protein analysis.
- RNA immunoprecipitation (RIP) and dual-luciferase reporter assays to confirm molecular interactions.
Main Results:
- Overexpression of hsa_circ_0021001 or GREM1 inhibited hBVSMC viability and migration, promoted apoptosis, and altered PCNA and α-SMA levels.
- miR-152-3p directly binds to GREM1 and hsa_circ_0021001, reversing the effects of hsa_circ_0021001.
- Inhibition of miR-152-3p impaired hBVSMC function, while GREM1 knockdown rescued these effects.
Conclusions:
- hsa_circ_0021001 modulates GREM1 expression through the miR-152-3p axis in hBVSMCs.
- This interaction regulates IA-associated phenotypic changes by affecting cell viability, migration, and apoptosis.
Abstract:
hsa_circ_0021001 is downregulated in intracranial aneurysm (IA), and this downregulation influences the growth of human brain vascular smooth muscle cells (hBVSMCs). However, the mechanism by which hsa_circ_0021001 contributes to hBVSMC dysfunction in IA remains unclear. In this study, the expressions of miR-152-3p, hsa_circ_0021001, and Gremlin 1 (GREM1) were detected using qRT-PCR. Cell viability was assessed using CCK-8 assays, protein levels of GREM1 and proliferating cell nuclear antigen (PCNA) were evaluated using western blotting. In addition, RNA immunoprecipitation (RIP) and dual-luciferase reporter assays were performed to validate the correlation among hsa_circ_0021001, GREM1, and miR-152-3p. Our results indicated that overexpression of hsa_circ_0021001 or GREM1 inhibited hBVSMC viability and migration, promoted cell apoptosis, decreased PCNA levels, and increased α-SMA levels. Additionally, miR-152-3p was shown to directly bind to both GREM1 and hsa_circ_0021001, reversing the effects of hsa_circ_0021001 on PCNA and α-SMA expression, hBVSMC viability, cell migration, and apoptosis. Inhibition of miR-152-3p suppressed hBVSMC viability and migration and promoted apoptosis, while GREM1 knockdwon rescued these cellular phenotypesthe and restored PCNA and α-SMA expression. In conclusion, hsa_circ_0021001 modulates GREM1 expression via miR-152-3p in hBVSMCs, thereby regulating IA-associated phenotypic alterations by suppressing cell viability and migration. It also promotes apoptosis through the miR-152-3p/GREM1 axis.
