Elevated plasma CaM expression in patients with acute cerebral infarction predicts poor outcomes and is inversely associated with miR-26b expression

Background: Calcium overload plays an important role in ischemia/reperfusion injury during ischemic brain damage and is mediated by calmodulin (CaM). However, the understanding of the regulatory mechanisms of CaM expression at the gene level is limited. The expression levels of miR-26b change significantly during ACI, and bioinformatic analyses predict that miR-26b would be a potential regulator of calmodulin (CALM1) mRNA. This study aimed to determine the expression of miR-26b and CaM in the plasma of patients with ACI and investigate the impact of miR-26b on CALM1 expression. Methods: CaM and miR-26b expression analyses from the plasma of patients with ACI and normal controls were performed using ELISA and qRT-PCR, respectively. Correlations between CaM, miR-26b, and NIHSS scores were analyzed. Then, miR-26b mimics and inhibitors were transfected into HUVE cell lines via lipofectamine. CALM1 mRNA expression in HUVECs was detected by RT-PCR, and the protein levels were detected by Western blot. Results: ...