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Transcriptome analysis of control and OTUD1 knockout SKOV3 Cells

ABSTRACT: Transcriptome analysis of control and OTUD1 knockout SKOV3 Cells

PROVIDER: PRJNA973961 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24637300_1.fastq.gz	Fastqsanger.gz
	SRR24637300_2.fastq.gz	Fastqsanger.gz
	SRR24637301_1.fastq.gz	Fastqsanger.gz
	SRR24637301_2.fastq.gz	Fastqsanger.gz
	SRR24637302_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of control and OTUD1 knockout SKOV3 Cells

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Transcriptome analysis of control and OTUD1 knockout T24 Cells

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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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Next Generation Sequencing of Transcriptomes in SKOV3 and rhCCL20-treated SKOV3 cells

Project description:The goals of this study are to compare the transcriptome differences between SKOV3 and rhCCL20-treated SKOV3 cells and identify the defferential expressed genes regulated by rhCCL20 in SKOV3 cells. We treated SKOV3 cells with 5% trehalose (control group) and rhCCL20 protein dissolved in 5% trehalose (experimental group) in vitro. The cells were collected 24 hours after treatment and used for RNA-sequencing.

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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.

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