Plasma miR-409-3p promotes acute cerebral infarction via suppressing CTRP3.

Abstract

Abnormal expression of miR-409-3p has been found in several neurodevelopmental disorders, but whether it is dysregulated in the patients with acute cerebral infarction (ACI) has not been evaluated. The current study mainly focused on the clinical significance and the underlying mechanism of plasma miR-409-3p in the progression of ACI. The level of plasma miR-409-3p was determined in ACI patients (n = 80) and healthy controls (n = 30). Pearson correlation assay was performed to evaluate the association and cardiovascular risk factors. A receiver operating characteristic curve (ROC) was used to evaluate the diagnostic value of plasma miR-409-3p levels in patients with ACI. Dual luciferase reporter assay and western blot were performed to determine the possible target gene of miR-409-3p. Our data showed that the expression of plasma miR-409-3p in the ACI group was higher than that in the healthy controls. Furthermore, Pearson correlation analysis indicated a positive correlation between plasma miR-409-3p and the NIHSS score. ROC analysis indicated that plasma miR-409-3p could differentiate plasma miR-409-3p in ACI patients from healthy controls. Then, we explored the possible target genes of miR-409-3p. Interestingly, C1q and TNF-related 3 (CTRP3), a novel adipose tissue-derived secreted factor, was found to be a target gene of miR-409-3p. We found that knockdown of CTRP3 significantly induced PC12 cell apoptosis, even in PC12 cells transfected with miR-409-3p inhibitor. These data suggested that miR-409-3p induced PC12 cell apoptosis by targeting CTRP3. Altogether, elevated plasma miR-409-3p is correlated with disease severity and may be efficient for the early diagnosis of ACI.