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

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

PROVIDER: PRJNA1010134 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25775953_1.fastq.gz	Fastqsanger.gz
	SRR25775953_2.fastq.gz	Fastqsanger.gz
	SRR25775954_1.fastq.gz	Fastqsanger.gz
	SRR25775954_2.fastq.gz	Fastqsanger.gz
	SRR25775955_1.fastq.gz	Fastqsanger.gz

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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

Gene expression profiles of ASK1-deficient adipose tissues

Project description:To elucidate the potential function of ASK1 in adipose tissues, microarray analysis was performed using iBAT and eWAT. Tissue samples were collected from 10-week-old male mice, and RNA samples derived from three individuals were pooled to analyze. These data provide novel insights into the physiological functions of ASK1. To elucidate the potential function of ASK1 in adipose tissues, microarray analysis was performed using iBAT and eWAT.

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Transcriptome analysis of control and OTUD1 knockout T24 Cells

Project description:We have confirmed that OTUD1 interacted directly with Akt and inhibited Akt phosphorylation. To investigate the exact mechanism of OTUD1 in the regulation of Akt signaling pathway, we established T24 cells with stable OTUD1 depletion by using sgRNA.

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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.

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Transcriptome analysis of control and OTUD1 knockout SKOV3 Cells

Project description:We have confirmed that high level of OTUD1 is important for retaining ovarian cancer stem cells (OCSCs) property. To investigate the exact mechanism of OTUD1 in the regulation of stemness maintain, we established SKOV3 cells with stable OTUD1 depletion by using sgRNA.

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Expression data from inflorescence (unopened flower buds) of Arabidopsis thaliana - comparison between Ler and ask1 mutant

Project description:ARABIDOPSIS SKP1-LIKE1 (ASK1) protein is involved in regulating flower development. We have compared ask1 mutant floral transcriptome with wild-type Ler to identify the role of ASK1-containing E3 ubiquitin ligases in regulating flower transcriptome. In this dataset, we include the expression data obtained from Arabidopsis thaliana Ler and ask1 mutant flower buds. We identified 42 genes and 74 genes that are down-regulated and up-regulated, respectively. Totally 5 samples were analyzed: 3 samples of ask1 and 2 samples of Ler. The average values were compared between ask1 and Ler.

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