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Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunction

ABSTRACT: Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunction

PROVIDER: PRJNA1231014 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR32554361_1.fastq.gz	Fastqsanger.gz
	SRR32554361_2.fastq.gz	Fastqsanger.gz

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Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

Project description:Understanding the molecular mechanisms of pathological vascular remodeling is important for treating cardiovascular diseases and complications. Recent studies have highlighted a role of deubiquitinases in vascular pathophysiology. In this study, we investigated the role of a deubiquitinase, OTUD1, in angiotensin II (Ang II)-induced vascular remodeling. We identified upregulated OTUD1 in the vascular endothelium of Ang II-challenged mice and showed OTUD1 deletion attenuated vascular remodeling, collagen deposition, and EndMT. Conversely, OTUD1 overexpression aggravated these pathological changes both in vivo and in vitro. Mechanistically, SMAD3 was identified as a substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. We found OTUD1 stabilizes SMAD3 and facilitates SMAD3/SMAD4 complex formation and subsequent nuclear translocation through both K48- and K63-linked deubiquitination. OTUD1-mediated SMAD3 activation regulate the transcription of genes involved in vascular EndMT and remodeling in HUVECs. Finally, SMAD3 inhibition reversed OTUD1-promoted vascular remodeling. Our findings demonstrate endothelial OTUD1 promoted Ang II-induced vascular remodeling by deubiquitinating SMAD3. This study identified SMAD3 as a target of OTUD1 and indicates OTUD1 as a potential therapeutic target for the diseases related to vascular remodeling.

2022-12-24 | GSE217304 | GEO

Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

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Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunction

Project description:To analyze the mRNA profile of DUBs in diabetic heart, we performed a scRNA-seq of heart cells from the wild type (WT) mice and db/db mice, a typical T2DM model mouse.

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OTUD1 aggravates pathological cardiac hypertrophy through activation of PGAM5-ASK1 signaling pathways

Project description:Deubiquitinating enzymes have gained more and more attention in the field of pathological cardiac hypertrophy. In this study, we explored the role of a deubiquitinase, OTUD1, in the transverse aortic constriction (TAC) induced cardiac hypertrophy. We found the upregulation of OTUD1 in heart tissues of TAC mice. OTUD1 overexpression promoted cardiac hypertrophy, cardiac fibrosis and apoptosis. Conversely, OTUD1 depletion alleviated these pathological changes both in vivo and in vitro. Mechanistically, ASK1 was identified as one substrate of OTUD1 using co-immunoprecipitation followed with LC-MS/MS. Interestingly, OTUD1 didn’t deubiquitinate ASK1, but increased the phosphorylation level of ASK1 during the process of cardiac hypertrophy. We found that PGAM5, the upper stream regulator of ASK1, was stabilized by OTUD1 in a K63 ubiquitin chain dependent way, which reminded us OTUD1 increased the phosphorylation level of ASK1 by deubiquitinating PGAM5. This study identified the OTUD1-ASK1 axis as a potential therapeutic target for pathological cardiac hypertrophy.

2023-09-05 | GSE241809 | GEO

Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

Project description:Endothelial OTUD1 promotes Ang II-induced vascular remodeling by deubiquitinating SMAD3

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Cardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunctionCardiomyocyte OTUD1 drives diabetic cardiomyopathy via directly deubiquitinating AMPKα2 to inhibit AMPK activity and induce mitochondrial dysfunction

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Increased response to mitochondrial uncoupling for lipid oxidation and reduced lipid synthesis in AMPKα2-/- myotubes

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AMPKα2 binds to chromatin to regulate gene expression in ALL cells [ChIP-seq]

Project description:To identify genome-wide genes regulated by direct association of AMPKα2 to chromatin, ChIP-Seq assays were performed using HA (HA-AMPKα2) and RPB1 (RNA Pol II) antibodies in CCRF-CEM/HA-AMPKα2 (CN2) cells treated with glucose deprivation or no treatment controls. ChIP-seq analysis identified around 600 genes to which loci AMPKα2 was directly bound; many of these genes with HA-AMPKα2 recruitment overlapped with genes exhibiting RNA Pol II enrichment.

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Transcriptome analysis of control and OTUD1 knockout T24 Cells

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