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Early activated ageing-related changes in cardiac transcriptome of Tgαq*44 mice during entire HF development

ABSTRACT: To investigate ageing-related changes in cardiac transcriptome of FVB mice we performed differential gene expression profiling analysis using data obtained from RNA-seq of five life time points (4-, 8-, 10-, 12-, 14 months) by comparing older FVB mice (8-, 10-, 12-, 14 months) to young 4-month-old FVB mice (FVB vs. FVB analysis). Genes that were differentially expressed in FVB vs. FVB analysis were also annotated to the respective biological processes based on Gene Ontology database, assessed for their overrepresentation to indicate processes involved in cardic ageing process in FVB mice. To investigate heart failure-related as well as ageing-related changes in cardiac transcriptome of Tgαq*44 mice we performed differential gene expression profiling analysis using data obtained from RNA-seq of five life time points (4-, 8-, 10-, 12-, 14 months) by comparing Tgαq*44 to age-matched FVB mice (Tgαq*44 vs. FVB analysis). Genes that were differentially expressed in Tgαq*44 vs. FVB analysis were also annotated to the respective biological processes based on Gene Ontology database, assessed for their overrepresentation to indicate processes iniciated along heart failure development as well as cardiac ageing process in Tgαq*44 mice. To investigate early activated ageing-related changes in cardiac transcriptome of Tgαq*44 mice during entire heart failure development we searched for the presence of ageing-related genes (those identified in cardiac transcriptome of older FVB mice) among genes which were differentially expressed commonly at each measured time points in Tgαq*44 vs. FVB analysis. To investigate early activated aging-related biological processes in cardiac transcriptome of Tgαq*44 mice during entire heart failure development, we searched for the presence of ageing-related processes (those identified in cardiac transcriptome of older FVB mice) among processes which were overrepresented commonly at each measured time points in Tgαq*44 vs. FVB analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE207648 | GEO | 2022/12/15

REPOSITORIES: GEO

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Project description:Muscle ring finger-1 (MuRF1) is a muscle-specific protein implicated in the regulation of cardiac myocyte size and contractility. MuRF2, a closely related family member, redundantly interacts with protein substrates, and hetero-dimerizes with MuRF1. Mice lacking either MuRF1 or MuRF2 are phenotypically normal whereas mice lacking both proteins develop a spontaneous cardiac and skeletal muscle hypertrophy indicating cooperative control of muscle mass by MuRF1 and MuRF2. In order to identify the role that MuRF1 plays in regulating cardiac hypertrophy in vivo, we created transgenic mice expressing increased amounts of cardiac MuRF1. Adult MuRF1 transgenic (Tg+) hearts exhibited a non-progressive thinning of the left ventricular wall and a concomitant decrease in cardiac function. Experimental induction of cardiac hypertrophy by trans-aortic constriction (TAC) induced rapid failure of MuRF1 Tg+ hearts. Microarray analysis identified that the levels of genes associated with metabolism (and in particular mitochondrial processes) were significantly altered in MuRF1 Tg+ hearts, both at baseline and during the development of cardiac hypertrophy. Surprisingly, ATP levels in MuRF1 Tg+ mice did not differ from wild type mice despite the depressed contractility following TAC. To explain this discrepancy between the ongoing heart failure and maintained ATP levels in MuRF1 Tg+ hearts, we compared the level and activity of creatine kinase (CK) between wild type and MuRF1 Tg+ hearts. Although mCK and CK-M/B protein levels were unaffected in MuRF1 Tg+ hearts, total CK activity was significantly inhibited. We conclude that MuRF1’s inhibition of CK activity leads to increased susceptibility to heart failure following TAC, demonstrating for the first time that MuRF1 regulates cardiac energetics in vivo. Keywords: Genetic modification, physiological manipulation. Three-condition experiment, MuRF1 Tg+ vs. WT mice. Biological replicates: 4 WT baseline, 3 MuRF1 Tg+ baseline, cardiac overpressure hypertrophy induced by trans-aortic banding at 1 week (3 WT, 3 MurF Tg) and 4 weeks (3 WT, 3 MurF Tg), hearts harvested. One replicate per array.

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Early activated ageing-related changes in cardiac transcriptome of Tgαq*44 mice during entire HF development

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