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Transcriptomic profiling of wild-type and TigarKO mouse hearts [RNA-Seq]

ABSTRACT: Myocardial infarction induces profound transcriptional remodeling in the heart, particularly affecting mitochondrial pathways. To characterize zone-specific transcriptomic responses, we performed RNA sequencing of infarct, border, and remote regions from wild-type (WT) and TKO mouse hearts following infarction. Analysis of infarct territories revealed extensive preservation of mitochondrial gene expression in TKO hearts compared with WT controls. In contrast, mitochondrial DNA–encoded gene expression showed no significant differences between WT and TKO hearts in either the border or remote zones. Similarly, expression of nuclear-encoded genes in the border and remote zones was largely unchanged between genotypes. Together, these data indicate that transcriptional differences between WT and TKO hearts are predominantly localized to the infarct region, while border and remote zones exhibit minimal genotype-dependent changes.

ORGANISM(S): Mus musculus

PROVIDER: GSE317048 | GEO | 2026/01/30

REPOSITORIES: GEO

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Project description:Myocardial infarction results in a massive loss of cardiomyocytes which will not be regenerated. Recent studies using models of regeneration show that cardiomyocytes at the border of the injury are most prone to proliferate. Which processes occur in this region and make these cells act as progenitors, remains to be elucidated. In addition, we lack molecular markers for the identification of these cells in the human heart. To create a transcriptional profile of the murine border zone, identifying local processes and enabling the discovery of marker genes which will allow the identification of human cardiomyocytes with potential proliferative capacity. Myocardial infarction (MI) was induced in mice and 3, 7 or 14 days later ventricular tissue was isolated ranging from the injured area into the remote myocardium. Tomo-sequencing was performed on these cardiac tissue samples, which comprises of tissue sectioning together with RNA-sequencing on individual sections. This resulted in spatially resolved transcriptome maps containing a dynamic, transcriptionally distinct border zone with reduced expression of genes involved in mitochondrial oxidative phosphorylation, fatty acid metabolism and sarcomere function and increased expression of myofibroblast and proliferation genes. Genes shared between the murine and zebrafish border zone, such as ANKRD1, UCHL1 and DES, were validated as molecular markers in injured human hearts. Unexpectedly, pronounced expression of these marker genes was found in surviving cardiomyocytes located at the sub-endocardium. The border zone is an evolutionary conserved, transcriptionally distinct and dynamic region. With the use of newly identified markers, we discovered the existence of sub-endocardial cardiomyocytes in ischemic human hearts that share transcriptional characteristics with potential progenitor cells. This might have far reaching implications for the development of strategies to stimulate the regenerative capacity of patients suffering from ischemic injury.

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Transcriptomic profiling of wild-type and TigarKO mouse hearts [RNA-Seq]

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