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Stress response factor ATF4 drives liver fibrosis by governing a stress-independent enhancer program to activate hepatic stellate cells

ABSTRACT: ATF4 promotes HSC activation and drives liver fibrosis independent of its canonical functions in stress signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE235786 | GEO | 2024/11/30

REPOSITORIES: GEO

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Stress response factor ATF4 drives liver fibrosis by governing a stress-independent enhancer program to activate hepatic stellate cells

Project description:Stress response factor ATF4 drives liver fibrosis by governing a stress-independent enhancer program to activate hepatic stellate cells

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ATF4 governs functional expansion of hematopoietic stem cells partially via Angptl3 in the fetal liver microenvironment (array)

Project description:In this study, we demonstrated that deletion of the activating transcription factor 4 (ATF4) resulted in severely impaired HSC expansion in the fetal liver at E12.5 and E15.5. In contrast, generation of the first HSC population in the aorta-gonad-mesonephros region at E11.5 was not significantly affected. Furthermore, the HSC-supporting ability of both endothelial and stromal cells in fetal liver was significantly compromised in the absence of ATF4. Gene profiling using RNA-seq revealed down-regulated expression of a panel of cytokines in ATF4-/- stromal cells, including angiopoietin-like protein 3 (Angptl3) and vascular endothelial growth factor-A (VEGFA). To investigate the molecular pathways of ATF4 in the stromal cells and LSK cells in the fetal liver.

2015-11-20 | E-GEOD-66381 | biostudies-arrayexpress

ATF4 governs functional expansion of hematopoietic stem cells partially via Angptl3 in the fetal liver microenvironment (RNA-Seq)

2015-11-20 | E-GEOD-66380 | biostudies-arrayexpress

ATF4 governs functional expansion of hematopoietic stem cells partially via Angptl3 in the fetal liver microenvironment (array)

2015-11-20 | GSE66381 | GEO

ATF4 governs functional expansion of hematopoietic stem cells partially via Angptl3 in the fetal liver microenvironment (RNA-Seq)

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Loss of ATF4 leads to functional aging-like attrition of adult hematopoietic stem cells [RNA-seq]

Project description:We collected significant amount of phenotypic and mechanistic data from a ATF4 knockout mouse model and demonstrated that HSC defects with an aging-like phenotype (expanded pool of phenotypical HSCs, decreased number of functional HSCs, impaired repopulating and self-renewal capacities of HSCs and myeloid bias) occurred in the ATF4 KO mice, suggesting that not only ATF4 indeed represents a pivotal factor for adult HSC function but also we had successfully constructed an ideal and attractive model to study aging and aging-related disease.

2021-12-29 | GSE132682 | GEO

Global proteome analysis of ATF4 targets during ER stress.

Project description:Cancer cells exploit many of the cellular adaptive responses to support their survival needs. One such critical pathway in eukaryotic cells is the unfolded protein response (UPR) that is important in normal physiology as well as disease states, including cancer. Since UPR can serve as a lever between survival and death, regulated control of its activity is critical for tumor formation and growth although the underlying mechanisms are poorly understood. Here we show that one of the main transcriptional effectors of UPR, activating transcription factor 4 (ATF4), is essential for prostate cancer (PCa) growth and survival. To identify ATF4 target genes that mediate the ISR outcome and to get insight into its mechanism of action in PCa, we performed global proteomic expression profiling in parallel with transcriptomic expression profiling. These data show that ATF4 regulates important metabolic pathways in PCa cells.

2019-07-22 | PXD012858 | Pride

Gene expression data of LT-HSC, MEP and CMP cells from Mx1cre;Atf4 fl/fl mice(cKO) BM and those from controls

Project description:To elucidate the mechanisms underlying the role of Atf4 deficiency in erythropoiesis, we performed RNA sequencing on LT-HSC, MEP and CMP cells from Atf4 hematopoietic cell-specific conditional knockout mice(cKO) and those from WT mice.

2024-03-15 | GSE233677 | GEO

Effect of muscle-specific ATF4 gene knockout (ATF4 mKO) on skeletal muscle mRNA levels in aged mice.

Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. Quadriceps femoris muscles were harvested from 22-month-old muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.

2015-09-03 | E-GEOD-72658 | biostudies-arrayexpress

Glycolysis in hepatic stellate cells coordinates fibrogenic extracellular vesicle release spatially to amplify liver fibrosis

Project description:Liver fibrosis is characterized by the activation of perivascular hepatic stellate cells (HSCs), the release of fibrogenic nano-sized extracellular vesicles (EVs) and increased HSC glycolysis. Nevertheless, how glycolysis in HSCs coordinates fibrosis amplification through tissue zone-specific pathways remains elusive. Here, we demonstrate that HSC-specific genetic inhibition of glycolysis reduced liver fibrosis. Moreover, spatial transcriptomics revealed a fibrosis-mediated upregulation of EV-related pathways in the liver pericentral zone, which was abrogated by the glycolysis genetic inhibition. Mechanistically, glycolysis in HSCs upregulated the expression of EV-related genes such as RAB31 by enhancing histone-3-lysine-9 acetylation on the promoter region, which increased EV release. Functionally, these glycolysis-dependent EVs increased fibrotic gene expression in recipient HSC. Furthermore, EVs derived from glycolysis-deficient mice abrogated liver fibrosis amplification in contrast to glycolysis-competent mouse EVs. In summary, glycolysis in HSCs amplifies liver fibrosis by promoting fibrogenic EV release in the hepatic pericentral zone, which represents a potential therapeutic target.

2024-05-16 | PXD050337 | Pride

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