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BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration

ABSTRACT: BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration

PROVIDER: PRJNA557213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9854934_1.fastq.gz	Fastqsanger.gz
	SRR9854934_2.fastq.gz	Fastqsanger.gz
	SRR9854935_1.fastq.gz	Fastqsanger.gz
	SRR9854935_2.fastq.gz	Fastqsanger.gz
	SRR9854936_1.fastq.gz	Fastqsanger.gz

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BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration

Project description:We report that BRG1, an ATPase subunit of the SWI/SNF chromatin remodeling complex, was required for the homeostatic maintenance of colonic epithelial cells (IECs) to prevent the inflammation and tumorigenesis. Consistent with the reduced BRG1 expression in IBD patients, adult mice with IEC ablation of BRG1 developed spontaneous colitis and exhibited increased susceptibility to mutagen-induced tumor growth. Conversely, BRG1 overexpression protected the mice from DSS-induced epithelial damage and subsequent oncogenesis. Mechanistically, BRG1 emerged as a key regulator that directly governs the transcription of Atg16l1, Ambra1, Atg7 and Wipi2, which are important for autophagosome biogenesis. Thus, defective autophagy in BRG1-deficient IECs resulted in excess reactive oxygen species (ROS), which led to the defects in cellular apoptosis and barrier integrity.

2019-09-09 | GSE135041 | GEO

BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration.

Project description:Autophagy is a central component of integrated stress responses that influences many inflammatory diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). While the core machinery is known, the molecular basis of the epigenetic regulation of autophagy and its role in colon inflammation remain largely undefined. Here, we report that BRG1, an ATPase subunit of the SWI/SNF chromatin remodeling complex, is required for the homeostatic maintenance of intestinal epithelial cells (IECs) to prevent the inflammation and tumorigenesis. BRG1 emerges as a key regulator that directly governs the transcription of Atg16l1, Ambra1, Atg7 and Wipi2, which are important for autophagosome biogenesis. Defective autophagy in BRG1-deficient IECs results in excess reactive oxygen species (ROS), which leads to the defects in barrier integrity. Together, our results establish that BRG1 may represent an autophagy checkpoint that is pathogenetically linked to colitis and is therefore likely a potential therapeutic target for disease intervention.

| S-EPMC6787222 | biostudies-literature

Protein-protein interactions of BRG1 or BRG1-HSA in SW13 cells

Project description:The SWI/SNF complex remodels chromatin in an ATP-dependent manner through the ATPase subunits BRG1 and BRM. Chromatin remodeling alters nucleosome structure to change gene expression, however aberrant remodeling and gene expression can result in cancer. The function and localization on chromatin of the SWI/SNF complex depends on the protein makeup of the complex. Here we report the protein-protein interactions of wild-type BRG1 or mutant BRG1 in which the HSA domain has been deleted (BRG1-HSA). We demonstrate the interaction of BRG1 with most SWI/SNF complex members and a failure of a number of these members to interact with BRG1-HSA. These results demonstrate that the HSA domain of BRG1 is a critical interaction platform for the correct formation of SWI/SNF remodeling complexes.

2023-02-15 | PXD029647 | Pride

NP-6A4 activates a novel signaling network of protective autophagy in obese female rat heart and attenuates cardiac dysfunction and coronary microvascular damage

Project description:NP-6A4 activates a novel signaling network of protective autophagy in obese female rat heart and attenuates cardiac dysfunction and coronary microvascular damage

2023-09-25 | PXD036596 | Pride

TBC1D2B undergoes phase separation and mediates autophagy initiation

Project description:Small ubiquitin-like modifiers from the ATG8 family regulate autophagy initiation and progression in mammalian cells. Their interaction with LC3-interacting region (LIR) containing proteins promotes cargo sequestration, phagophore assembly, or even fusion between autophagosomes and lysosomes. Previously, we have shown that RabGAP proteins from the TBC family directly bind to LC3/GABARAP proteins. In the present study, we focus on the function of TBC1D2B. We show that TBC1D2B contains a functional canonical LIR motif and acts at an early stage of autophagy by binding to both LC3/GABARAP proteins and ATG5 conjugation machinery. Subsequently, TBC1D2B is degraded by autophagy. TBC1D2B condensates into liquid droplets upon autophagy induction. Our study suggests that phase separation is an underlying mechanism of TBC1D2B-dependent autophagy induction, which serves as an assembly platform for further cargo sequestration.

2023-09-28 | PXD039959 | Pride

MYTHO: a novel regulator of skeletal muscle autophagy and integrity

Project description:Autophagy is a critical process in the regulation of muscle mass, function and integrity. The molecular mechanisms regulating autophagy are complex and still partly understood. Here, we identify and characterize a novel FoxO-dependent gene, d230025d16rik which we named Mytho (Macroautophagy and YouTH Optimizer), as a regulator of autophagy and skeletal muscle integrity in vivo. Mytho is significantly up-regulated in various mouse models of skeletal muscle atrophy. Short term depletion of MYTHO in mice attenuates muscle atrophy caused by fasting, denervation, cancer cachexia and sepsis. While MYTHO overexpression is sufficient to trigger muscle atrophy, MYTHO knockdown results in a progressive increase in muscle mass associated with a sustained activation of the mTORC1 signaling pathway. Prolonged MYTHO knockdown is associated with severe myopathic features, including impaired autophagy, muscle weakness, myofiber degeneration, and extensive ultrastructural defects, such as accumulation of autophagic vacuoles and tubular aggregates. Inhibition of the mTORC1 signaling pathway in mice using rapamycin treatment attenuates the myopathic phenotype triggered by MYTHO knockdown. Skeletal muscles from human patients diagnosed with myotonic dystrophy type 1 (DM1) display reduced Mytho expression, activation of the mTORC1 signaling pathway and impaired autophagy, raising the possibility that low Mytho expression might contribute to the progression of the disease. We conclude that MYTHO is a key regulator of muscle autophagy and integrity.

2023-01-20 | GSE222885 | GEO

Angiotensin IV attenuates diabetic cardiomyopathy via suppressing FoxO1-induced excessive autophagy, apoptosis and fibrosis

Project description:Angiotensin IV attenuates diabetic cardiomyopathy via suppressing FoxO1-induced excessive autophagy, apoptosis and fibrosis

| PRJNA660959 | ENA

TFEB activation in macrophages attenuates postmyocardial infarction ventricular dysfunction independently of ATG5-mediated autophagy

Project description:TFEB activation in macrophages attenuates postmyocardial infarction ventricular dysfunction independently of ATG5-mediated autophagy

| PRJNA485726 | ENA

Transcriptional profiling of Lung H1299-BRG1 inducible cells

Project description:Global Transcriptional analysis of BRG1 in lung cancer cells Comparative transcriptional profile comparing the expression in lung cancer cells before and after restoring the wild type BRG1 or mutant BRG1 expression controlled by the Tet-ON system (doxycycline depending expression)

2012-03-12 | E-GEOD-35168 | biostudies-arrayexpress

Rescue Of Dysfunctional Autophagy By Peptide IDR-1018 Attenuates Hyperinflammatory Phenotype Of Cystic Fibrosis Cells (RNA-seq)

Project description:Genome-wide gene expression was measured in peripheral blood mononuclear cells (PBMCs) from patients with cystic fibrosis (CF) after treatment in vitro with the flagellin protein fliC, and/or synthetic peptide IDR-1018 to assess patterns of gene expression. The patterns of gene expression suggest that CF cells have a hyperinflammatory phenotype including dysfunctional autophagy processes. The synthetic peptide IDR-1018 attentuates this hyperinflammatory phenotype. Total RNA was obtained from PBMCs obtained from CF patients after treatment with the fliC flagellin protein (that is known to play a role in CF lung inflammation), and/or the peptide IDR-1018 that has anti-inflammatory properties. Comparison of genes and pathways affected by these treatments indicated the role of autophagy process in CF disease.

2012-11-20 | E-GEOD-35394 | biostudies-arrayexpress

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