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BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss

ABSTRACT: BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss

PROVIDER: PRJNA1019260 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26117345_1.fastq.gz	Fastqsanger.gz
	SRR26117345_2.fastq.gz	Fastqsanger.gz
	SRR26117346_1.fastq.gz	Fastqsanger.gz
	SRR26117346_2.fastq.gz	Fastqsanger.gz
	SRR26117347_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss

Project description:The apical-basal polarity of pancreatic acinar cells is essential for maintaining tissue architecture. However, the mechanisms by which polarity proteins regulate acinar pancreas tissue homeostasis are poorly understood. Here, we evaluate the role of Par3 in acinar pancreas injury and homeostasis. While Par3 loss in the mouse pancreas disrupts tight junctions, Par3 loss is dispensable for pancreatogenesis. However, with aging, Par3 loss results in low-grade inflammation, acinar degeneration, and pancreatic lipomatosis. Par3 loss also exacerbates pancreatitis-induced acinar cell loss, resulting in pronounced pancreatic lipomatosis and failure to regenerate. Moreover, Par3 loss in mice harboring mutant Kras causes extensive pancreatic intraepithelial neoplastic (PanIN) lesions and large pancreatic cysts. We also show that Par3 loss restricts injury-induced primary ciliogenesis. Significantly, targeting BET proteins enhances primary ciliogenesis during pancreatitis-induced injury and, in mice with Par3 loss, limits pancreatitis-induced acinar loss and facilitates acinar cell regeneration. Combined, this study demonstrates how Par3 restrains pancreatitis- and Kras-induced changes in the pancreas and identifies a potential role for BET inhibitors to attenuate pancreas injury and facilitate pancreas tissue regeneration.

2024-08-05 | GSE243623 | GEO

BET inhibition rescues ciliogenesis and ameliorates pancreatitis-driven phenotypic changes in mice with Par3 loss.

| S-EPMC10515915 | biostudies-literature

Blockade of the Protease ADAM17 Ameliorates Experimental Pancreatitis

Project description:Blockade of the Protease ADAM17 Ameliorates Experimental Pancreatitis

| PRJNA886653 | ENA

Blockade of the Protease ADAM17 Ameliorates Experimental Pancreatitis

Project description:Acute and chronic pancreatitis, the latter associated with fibrosis, are multifactorial inflammatory disorders and leading causes of gastrointestinal disease-related hospitalisation, including death. Despite the global health burden of pancreatitis, currently there are no effective therapeutic agents. In this regard, the protease A Disintegrin And Metalloproteinase 17 (ADAM17) mediates inflammatory responses through shedding of bioactive inflammatory cytokines and mediators, including tumour necrosis factor α (TNFα) and the soluble interleukin (IL)-6 receptor (sIL-6R), the latter of which drives proinflammatory IL-6 trans-signalling. However, the role of ADAM17 in pancreatitis is unclear. To address this, Adam17ex/ex mice – which are homozygous for the hypomorphic Adam17ex allele resulting in marked reduction in ADAM17 expression – and their wild-type (WT) littermates were exposed to the cerulein-induced acute pancreatitis model, and acute (1-week) and chronic (20-weeks) pancreatitis models induced by the cigarette smoke carcinogen nicotine-derived nitrosamine ketone (NNK). Our data reveal that ADAM17 expression was upregulated in pancreatic tissues of animal models of pancreatitis. Moreover, the genetic (Adam17ex/ex mice) and therapeutic (ADAM17 prodomain inhibitor; A17pro) targeting of ADAM17 ameliorated experimental pancreatitis, which was associated with a reduction in the IL-6 trans-signalling/STAT3 axis. This led to reduced inflammatory cell infiltration, including T cells and neutrophils, as well as necrosis and fibrosis in the pancreas. Furthermore, upregulation of the ADAM17/IL-6 trans-signalling/STAT3 axis was a feature of pancreatitis patients. Collectively, our findings indicate that the ADAM17 protease plays a pivotal role in the pathogenesis of pancreatitis, which could pave the way for devising novel therapeutic options to be deployed against this disease.

2022-10-06 | GSE214666 | GEO

Inhibition of BET proteins rescues neural defects in Rett syndrome

Project description:Inhibition of BET proteins rescues neural defects in Rett syndrome

| PRJNA482365 | ENA

Inhibition of BET proteins rescues neural defects in Rett syndrome [ATAC-seq]

Project description:Inhibition of BET proteins rescues neural defects in Rett syndrome [ATAC-seq]

| PRJNA482370 | ENA

Inhibition of BET proteins rescues neural defects in Rett syndrome [HiC-seq]

Project description:Inhibition of BET proteins rescues neural defects in Rett syndrome [HiC-seq]

| PRJNA482373 | ENA

Inhibition of BET proteins rescues neural defects in Rett syndrome [ChIP-seq]

Project description:Inhibition of BET proteins rescues neural defects in Rett syndrome [ChIP-seq]

| PRJNA482369 | ENA

Inhibition of BET proteins rescues neural defects in Rett syndrome [scRNA-seq]

Project description:Inhibition of BET proteins rescues neural defects in Rett syndrome [scRNA-seq]

| PRJNA482371 | ENA

Inhibition of BET proteins rescues neural defects in Rett syndrome [RNA-seq]

Project description:Inhibition of BET proteins rescues neural defects in Rett syndrome [RNA-seq]

| PRJNA482372 | ENA

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