Activation of Galectin-3 (LGALS3) Transcription by Injurious Stimuli in the Liver Is Commonly Mediated by BRG1

Li, Zilong; Lv, Fangqiao; Dai, Congxin; Wang, Qiong; Jiang, Chao; Fang, Mingming; Xu, Yong

doi:10.3389/fcell.2019.00310

Cited by 35 publications

(31 citation statements)

References 87 publications

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“…Chromatin Immunoprecipitation (ChIP) assays were performed essentially as described before 47,[66][67][68][69][70][71][72][73][74][75][76][77][78][79][80] . In brief, chromatin in control and treated cells were cross-linked with 1% formaldehyde for 8 min at room temperature, and then sequentially washed with ice-cold phosphate-buffered saline, Solution I (10 mM HEPES, pH 7.5, 10 mM EDTA, 0.5 mM EGTA, 0.75% Triton X-100), and Solution II (10 mM HEPES, pH 7.5, 200 mM NaCl, 1 mM EDTA, 0.5 mM EGTA).…”

Section: Chromatin Immunoprecipitation (Chip)mentioning

confidence: 99%

Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion

et al. 2020

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TC10-like (TCL) is a small GTPase that has been implicated in carcinogenesis. Elevated TCL expression has been observed in many different types of cancers although the underlying epigenetic mechanism is poorly understood. Here we report that TCL up-regulation was associated with high malignancy in both human colorectal cancer biopsy specimens and in cultured colorectal cancer cells. Hypoxia, a pro-metastatic stimulus, up-regulated TCL expression in HT-29 cells. Further studies revealed that myocardin-related transcription factor A (MRTF-A) promoted migration and invasion of HT-29 cells in a TCL-dependent manner. MRTF-A directly bound to the proximal TCL promoter in response to hypoxia to activate TCL transcription. Chromatin immunoprecipitation (ChIP) assay showed that hypoxia stimulation specifically enhanced acetylation of histone H4K16 surrounding the TCL promoter, which was abolished by MRTF-A depletion or inhibition. Mechanistically, MRTF-A interacted with and recruited the H4K16 acetyltransferase hMOF to the TCL promoter to cooperatively regulate TCL transcription. hMOF depletion or inhibition attenuated hypoxia-induced TCL expression and migration/invasion of HT-29 cells. In conclusion, our data identify a novel MRTF-A-hMOF-TCL axis that contributes to colorectal cancer metastasis.

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Section: Chromatin Immunoprecipitation (Chip)mentioning

confidence: 99%

Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion

et al. 2020

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“…Chromatin immunoprecipitation (ChIP) assays were performed essentially as described before ( Li et al, 2019b ). In brief, chromatin in control and treated cells were cross-linked with 1% formaldehyde.…”

Section: Methodsmentioning

confidence: 99%

BRG1 Stimulates Endothelial Derived Alarmin MRP8 to Promote Macrophage Infiltration in an Animal Model of Cardiac Hypertrophy

Zhang

et al. 2020

Front. Cell Dev. Biol.

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Endothelial cell derived angiocrine factors contribute to the disruption of homeostasis and the pathogenesis of cardiovascular diseases in response to stress stimuli. In the present study we investigated the role of BRG1, a key component of the chromatin remodeling complex, in the regulation of angiocrine signaling. We report that angiotensin II (Ang II) induced pathological cardiac hypertrophy was attenuated in mice with endothelial-specific ablation of BRG1 (ecKO) compared to the control mice (WT). Mitigation of cardiac hypertrophy as a result of BRG1 deficiency was accompanied by decreased macrophage homing to the hearts. This could be explained by the observation that the ecKO mice exhibited down-regulation of myeloid-related protein 8 (MRP8), a well-established chemokine for macrophages, in vascular endothelial cells compared to the WT mice. Further analysis revealed that BRG1 mediated the activation of MRP8 expression by Ang II treatment in endothelial cells to promote macrophage migration. BRG1 was recruited to the MRP8 promoter by interacting with hypoxia-inducible factor 1 (HIF-1α). Reciprocally, BRG1 facilitated the binding of HIF-1α to the MRP8 promoter by sequentially recruiting histone acetyltransferase p300 and histone demethylase KDM3A. Depletion of either p300 or KDM3A repressed the induction of MRP8 expression by Ang II and ameliorated macrophage migration. In conclusion, our data delineate a novel epigenetic pathway whereby Ang II stimulates MRP8 production and macrophage homing to promote cardiac hypertrophy.

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“…PFI-3 treatment increased the accessibility of an mSWI/SNF-repressed promoter and its gene expression(90). In these and other studies, PFI-3 altered both gene expression patterns dependent on mSWI/SNF bromodomaincontaining proteins and the cellular and organismal phenotypes controlled by those genes(87,88,(91)(92)(93)(94)(95)(96). The data indicate that the pleiotropic effects of PFI-3 and inhibition of mSWI/SNF bromodomains links to the ability of the chromatin remodeling enzyme to modulate gene expression.In the realm of tissue specification, PFI-3 treatment caused a loss of "stemness" and promoted differentiation of ESCs and trophoblast and neural stem cells in the absence of differentiation signaling(41,97).…”

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confidence: 62%

The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation

Sharma

Witwicka

2020

Preprint

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Skeletal muscle differentiation induces changes in the epigenome of myoblasts as they proceed towards a myogenic phenotype. mSWI/SNF chromatin remodeling enzymes coordinate with lineage-determining transcription factors and are key regulators of differentiation. Three mSWI/SNF proteins, the mutually exclusive ATPases, BRG1 and BRM, and the BAF180 protein (Polybromo1, PBRM1) contain bromodomains belonging to the same structural subfamily. Bromodomains bind to acetylated lysines on histone N-terminal tails and on other proteins. Pharmacological inhibition of mSWI/SNF bromodomain function using the selective inhibitor PFI-3 reduced differentiation, decreased expression of myogenic genes, and increased the expression of cell cycle-related genes and the number of cells that remained in the cell cycle. Knockdown of BAF180 had no effect on differentiation, suggesting that only the BRG1 and BRM bromodomains contributed to differentiation. Comparison with existing gene expression data from myoblasts subjected to knockdown of BRG1 or BRM showed that bromodomain function was required for a subset of BRG1- and BRM-dependent gene expression. ChIP analysis revealed decreased BRG1 and BRM binding to target gene promoters, indicating that the BRG1 and BRM bromodomains promote chromatin binding. Thus mSWI/SNF ATPase bromodomains contribute to cell cycle exit, to skeletal muscle-specific gene expression, and to stable promoter binding by the mSWI/SNF ATPases.

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Activation of Galectin-3 (LGALS3) Transcription by Injurious Stimuli in the Liver Is Commonly Mediated by BRG1

Cited by 35 publications

References 87 publications

Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion

Epigenetic activation of the small GTPase TCL contributes to colorectal cancer cell migration and invasion

BRG1 Stimulates Endothelial Derived Alarmin MRP8 to Promote Macrophage Infiltration in an Animal Model of Cardiac Hypertrophy

The Bromodomains of the mammalian SWI/SNF (mSWI/SNF) ATPases Brahma (BRM) and Brahma Related Gene 1 (BRG1) promote chromatin interaction and are critical for skeletal muscle differentiation

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