Abstract
Circular RNAs (circRNAs) play a critical role in acute cerebral infarction (ACI). Our research discussed the effect of circ-Carm1 in ACI and its potential molecular mechanisms. Healthy controls and patients with ACI were included in this study. The establishment of an oxygen and glucose deprivation/reoxygenation (OGD/R) model of HT22 cells was conducted to mimic ACI in vitro. Quantitative reverse transcription polymerase chain reaction was conducted to determine mRNA levels extracted from serum and HT22 cell samples, and Western blotting was performed to determine protein levels. Terminal deoxynucleotidyl transferase dUTP nick end labeling and cell counting kit 8 assays were conducted to evaluate cellular functions. Concentrations of Fe2+ and malondialdehyde, and levels of transferrin receptor 1, glutathione peroxidase 4, and glutathione were evaluated to determine ferroptosis in OGD/R-induced HT22 cells. The binding relationships between mRNAs and miRNAs were verified. circ-Carm1 was highly expressed in OGD/R-treated HT22 cells. Deficiency of circ-Carm1 restored cell viability and suppressed ferroptosis in OGD/R-induced HT22 cells. miR-3098-3p was predicted to be a target of circ-Carm1. The miR-3098-3p inhibitor partly neutralized the functions of circ-Carm1 in OGD/R-induced HT22 cells. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) was confirmed to be a downstream target of miR-3098-3p and was elevated in OGD/R-induced HT22 cells. Overexpression of ACSL4 mitigated the functions of miR-3098-3p and accelerated HT22 cell dysfunction. Hence, circ-Carm1 is upregulated in ACI. circ-Carm1 suppression protects HT22 cells from dysfunction by inhibiting ferroptosis. Therefore, inducing circ-Carm1 deficiency may be a promising therapeutic method for ACI.