Expression profile of BAT from TAC-operated mice
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ABSTRACT:
PROVIDER: PRJNA702990 | ENA |
REPOSITORIES: ENA
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2025-04-06 | GSE288779 | GEO
Project description:<p>Background: Heart failure with reduced ejection fraction (HFrEF) is characterized by impaired contractility and high mortality. Dysregulation of intracellular ion cycling underlies the decline in cardiac contractility. Modulation of cardiac Na+/H+ and Ca2+ handling is considered a valuable approach for restoring cardiac function; thus, an in-depth understanding of the molecular regulation is timely for the discovery of new strategies to treat HFrEF.</p><p>Methods: Cardiac tissues from HFrEF patients and mice subjected to transverse aortic constriction (TAC) were analyzed for sterol regulatory element-binding protein 1 (SREBP1) transactivation of Sodium-hydrogen exchanger 3 (NHE3).Cardiomyocyte-specific SREBP1 transgenic (Srebp1a-Tg) and knockdown (Cre-Srebp1f/f) mice were generated. AAV9 vectors carrying Slc9a3 (encoding NHE3), Srebf1 or shRNA against Slc9a3, driven by the cardiomyocyte-specific cTnT promoter, were used to validate the role of the SREBP1-NHE3 in HFrEF. </p><p>Results: SREBP1 was activated in human hearts with HFrEF (dilated cardiomyopathy without diabetes or hyperlipidemia) and in mouse hearts with TAC-induced HFrEF. Srebp1a-Tg mice exhibited impaired cardiac contractilitywith dysregulated calcium handling in cardiomyocytes without apparent lipid accumulation. Transcriptomics analysis, ChIP-seq, ChIP assay, and promoter activity assessment showed that Slc9a3 (encoding NHE3) is a transcriptional target of SREBP1. Consistently, NHE3 was upregulated in Srebp1a-Tg mouse hearts, hearts under TAC surgery, and human failing hearts. Cardiomyocyte-specific knockdown of Srebp1 or Slc9a3 restored calcium handling and improved cardiac function in TAC hearts. In Srebp1a-Tg mice, NHE3 knockdown alleviated Na+ and Ca2+ overload and rescued cardiac systolic dysfunction. Conversely, NHE3 overexpression caused contractile impairment in both Cre-Srebp1f/f mice and controls, which offset the protective effect due to SREBP1 loss in the context of Na+ and Ca2+ overload. These resultsdemonstrate that SREBP1 upregulation of NHE3 caused cardiac dysfunction. Notably, empagliflozin downregulated NHE3 via AMP-activated protein kinase activation and inhibition of SREBP1, which ameliorated calcium overload and restored cardiac systolic function.</p><p>Conclusions: SREBP1 transactivates cardiac NHE3 expression during the progression of HFrEF, leading to dysregulatedcalcium handling and impaired contractility, suggesting a non-canonical role of SREBP1 in heart failure. Empagliflozin mitigates these detrimental effects by inhibiting the cardiac SREBP1-NHE3 axis, thus revealing a new pharmacological mechanism by which SGLT2i alleviates HF.</p>
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Project description:To study the gene expression profiles of brown (BAT) and white (WAT) adipose tissues in wild type and LR11-deficeint mice. The four RNA sources, WT scWAT, Lr11 -/- scWAT, WT BAT and Lr11 -/- BAT, were prepared from subcutaneous WAT and BAT from wild-type mice and Lr11 -/- mice, respectively (n=3 each).
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