ArticleAmerican journal of translational research2026
hsa_circ_0021001 modulates human brain vascular smooth muscle cell viability in intracranial aneurysm through the miR-152-3p/GREM1 axis.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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
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