AI Article Synopsis

  • Myocardial infarction (MI) leads to significant changes in gene expression across different heart cell types, which can be studied using single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing (RNA-seq) data.
  • In the analysis, decreased endothelial cells and increased macrophages were observed in MI, along with unique fibroblast subgroups showing varied responses, while specific apoptotic and ferroptotic genes were significantly upregulated in this context.
  • The findings highlight alterations in cardiac cell transcription during MI, confirming endothelial cell depletion, increased apoptosis markers in macrophages, and distinct gene expression patterns linked to ferroptosis, providing insights into the molecular processes involved in heart injury.

Article Abstract

Background: Myocardial infarction (MI) induces complex transcriptional changes across diverse cardiac cell types. Single-cell RNA sequencing (scRNA-seq) provides an unparalleled ability to discern cellular diversity during infarction, yet the veracity of these discoveries necessitates confirmation. This investigation sought to elucidate MI mechanisms by integrating scRNA-seq and bulk RNA-seq data.

Methods: Publicly available scRNA-seq (GSE136088) and bulk RNA-seq (GSE153485) data from mice MI models were analyzed. Cell types were annotated, and differential expression analysis conducted. Bulk RNA-seq underwent quality control, principal component analysis, and differential expression analysis.

Results: In scRNA-seq data, the comparison between MI and sham groups unveiled a reduction in endothelial cell populations, but macrophages and monocytes increased. Within fibroblast subgroups, three distinct categories were discerned, with two exhibiting upregulation in MI. Notably, endothelial cells exhibited an elevated expression of genes associated with apoptosis and ferroptosis. In bulk RNA-seq analysis, distinct patterns emerged when comparing MI and sham groups. Specifically, six genes linked to endothelial ferroptosis exhibited heightened expression in MI group, thereby corroborating the scRNA-seq findings. Moreover, the examination of isolated cardiac macrophages from mice MI model revealed increased expression of Spp1, Col1a2, Col3a1, Ctsd, and Lgals3 compared to sham group, thus substantiating the dysregulation of macrophage apoptosis-related proteins following MI.

Conclusion: MI altered the transcriptomic landscapes of cardiac cells with increased expression of apoptotic genes. Moreover, the upregulation of macrophage apoptosis marker was confirmed within MI models. The presence of endothelial cell depletion and ferroptosis in MI has been demonstrated.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448016PMC
http://dx.doi.org/10.1186/s12864-024-10813-1DOI Listing

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