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Updated: Jul 17, 2026
Preparation of a Non-Cardiomyocyte Cell Suspension for Single-Cell RNA Sequencing from a Post-Myocardial Infarction Adult Mouse Heart
Published on: February 3, 2023
Application of acute myocardial infarction-related key genes in noninvasive diagnosis: a comprehensive analysis based
Mingbin Xie1, Yuanhong Wu1, Xinyao Jin1
1Department of Cardiology, Hangzhou Red Cross Hospital, Hangzhou, Zhejiang, China.
Background:
Acute myocardial infarction (AMI), a highly fatal cardiovascular emergency, presents ongoing clinical challenges in both early diagnosis and the elucidation of its associated immuno-inflammatory processes. By integrating multi-omics data, this research seeks to identify novel diagnostic biomarkers and uncover their potential mechanisms in AMI.
Methods:
By integrating transcriptomic data, core genes linked to AMI were identified by differential expression and weighted gene co-expression network analysis (WGCNA). A multivariate logistic regression diagnostic model was constructed based on these genes, and its diagnostic efficacy was evaluated with receiver operating characteristic (ROC) curve analysis. In vitro, an oxygen-glucose deprivation/reperfusion (OGD/R) model was generated in AC16 human cardiomyocytes. We used lentiviral transduction to knock down the key gene. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay, apoptosis levels were measured by Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and flow cytometry, and the mRNA and protein expression of key genes were detected with qRT-PCR and Western blot.
Results:
Three AMI core genes (PLA2G15, ADAP2, and FAM20C) were successfully identified. The diagnostic model established via multifactorial logistic regression exhibited satisfactory discriminatory power. In vitro experiments confirmed that ADAP2 expression was markedly upregulated in the OGD/R model. Knocking down ADAP2 effectively alleviated OGD/R-induced suppression of cell proliferation, apoptosis enhancement, and expression increase of inflammatory factors (TNF-α, IL-6, IL-1β). Mechanistically, ADAP2 knockdown inhibited the expression of key proteins in the IL-17 signaling pathway (IL-17A, IL-17RA, ACT1). Exogenous addition of rhIL-17A reversed the protective effect of ADAP2 knockdown against cellular injury.
Conclusion:
The combined diagnostic model derived from the AMI core genes PLA2G15, ADAP2, and FAM20C exhibited robust diagnostic power for noninvasive diagnosis. ADAP2 can influence AMI-induced myocardial injury through the IL-17 signaling pathway.
