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Transcriptome analysis of heart tissue in wild type and cTnI R193H mutation mice based on RNA-seq

ABSTRACT: Aim:To explore the pathogenesis of restrictive cardiomyopathy (RCM) with cTnI mutation by using RNA-Seq to detect differentially expressed genes in WT and cardiac troponin I (cTnI) mutation mouse heart. Methods: The heart of WT mice and cTnI 193H mutant mice were extracted, all mRNA of myocardial tissue was extracted, and then transcribed into cDNA. After PCR amplification, the library was constructed, and high-throughput sequencing was performed. The sequencing results were analyzed to find the differentially expressed gene, and bioinformatics method was used to analyze the biological processes among those differentially expressed genes might be involved in. Results:A total of 52 differentially expressed genes were identified including 28 highly expressed and 24 low expressed ones ,of which 42 mRNA genes were differentially expressed (P<0.05). A total of 16 KEGG pathways were involved, and mainly participated in the immunological and metabolic processes. Conclusions:cTnI mutation may cause gene differential expression. Immune response,mitochondrial energy metabolism and myocardial cell differentiation may be involved in the progress of restrictive cardiomyopathy.The results might have offered new ideas for the research of RCM pathogenic mechanism.

ORGANISM(S): Mus musculus

PROVIDER: GSE146355 | GEO | 2023/02/28

REPOSITORIES: GEO

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Project description:Heart failure is associated with high morbidity and mortality and its incidence increases worldwide. MicroRNAs (miRNAs) are potential markers and targets for diagnostic and therapeutic applications, respectively. We determined myocardial and circulating miRNA abundance and its changes in patients with stable and end-stage heart failure before and at different time points after mechanical unloading by a left ventricular assist device (LVAD) by small-RNA-sequencing. MiRNA changes in failing heart tissues partially resembled that of fetal myocardium. Consistent with prototypical miRNAM-bM-^@M-^Starget-mRNA interactions, target mRNA levels were negatively correlated to changes in abundance for highly expressed miRNAs in heart failure and fetal hearts. The circulating small RNA profile was dominated by miRNAs, and fragments of tRNAs and small cytoplasmic RNAs. Heart- and muscle-specific circulating miRNAs (myomirs) increased up to 140-fold in advanced heart failure, which coincided with a similar increase in cardiac troponin I protein, the established marker for heart injury. These extracellular changes nearly completely reversed 3 months following initiation of LVAD support. In stable heart failure, circulating miRNAs showed less than 5-fold differences compared to normal, and myomir and cardiac troponin I levels were only captured near the detection limit. These findings provide the underpinning for miRNA-based therapies and emphasize the usefulness of circulating miRNAs as biomarkers for heart injury performing similar to established diagnostic protein biomarkers. Total RNA isolated from human left ventricular myocardium of failing hearts due to dilated or ischemic cardiomyopathy before and after mechanical unloading by a left ventricular assist device, and fetal myocardium compared to non-failing postnatal myocardium was subjected to multiplexed small RNA-sequencing on the Illumina platform. mRNA gene expression data using Illumina HumanHT-12v4 beadarrays for a subset of the myocardial samples is available (GSE52601).

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Transcriptome analysis of heart tissue in wild type and cTnI R193H mutation mice based on RNA-seq

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