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The influence of PRNCR1 rs1456315 polymorphism and PRNCR1 expression on myocardial infarction
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DOI：10.1186/s40001-026-04987-5.png)
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Abstract
En 中文
Myocardial infarction (MI) is a serious cardiovascular disease that endangers human life safety and imposes a heavy burden on global public health. This study aims to explore the influence of the PRNCR1 rs1456315 polymorphism and PRNCR1 expression on MI. This study included 144 non-MI volunteers and 185 MI patients. RT–qPCR and TaqMan–qPCR were used to detect the PRNCR1 level and the genotype distribution of PRNCR1 rs1456315. The correlation between PRNCR1 expression and clinical factors was analyzed by the chi-square test. The multivariate and univariate logistic regressions were used to analyze the risk factors in MI. The cell damage in hypoxic H9c2 and AC16 cells was detected by cell viability and LDH enzymatic activity. The dual luciferase assay was used to verify the targeting relationship. The PRNCR1 rs1456315 GG genotype and the G gene frequency were highly distributed in MI patients. The expression of PRNCR1 and FOXC1 was upregulated, and miR-9-3p was decreased in MI patients. Hyperlipidemia, TG, cholesterol, HDL, LDL, and hs-CRP were related to the PRNCR1 expression. Multivariate logistic regression indicated that the high PRNCR1 expression and the rs1456315 GG genotype were risk factors for MI. In vitro experiments, the expression of PRNCR1 and FOXC1 was upregulated, while miR-9-3p was reduced in hypoxic H9c2 and AC16 cardiomyocytes. The H9c2 and AC16 cells damage was alleviated by inhibiting PRNCR1, and inhibiting miR-9-3p reversed the effect of inhibiting PRNCR1. The PRNCR1 rs1456315 GG genotype may be a susceptibility factor for MI. PRNCR1 regulated the miR-9-3p/FOXC1 signaling axis, affecting hypoxia-induced myocardial cell damage.
Keywords:
Myocardial infarction
PRNCR1 rs1456315
MiR-9-3p
FOXC1
Hypoxia
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