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ASIC3-M-CSF-M2 macrophage-positive feedback loop modulates in skin fibrosis pathogenesis

ABSTRACT: ASIC3-M-CSF-M2 macrophage-positive feedback loop modulates in skin fibrosis pathogenesis

PROVIDER: PRJNA775894 | ENA |

REPOSITORIES: ENA

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ASIC3-M-CSF-M2 macrophage-positive feedback loop modulates in skin fibrosis pathogenesis

Project description:Inflammation is one of the main pathological features leading to skin fibrosis and a key factor leading to the progression of skin fibrosis. Acidosis caused by a decrease in extracellular pH is a sign of the inflammatory process. Acid-sensing ion channels (ASICs) are ligand-gated ion channels on the cell membrane that sense the drop in extracellular pH. However, the molecular mechanisms by which skin fibroblasts are regulated by Acid-sensing ion channel 3(ASIC3) remain unknown. This study investigated whether ASIC3 is related to inflammation and skin fibrosis and explored the underlying mechanisms. We demonstrate that Macrophage colony-stimulating factor (M-CSF) is a direct target of ASIC3, and ASIC3 activation promotes M-CSF transcriptional regulation of macrophages for M2 polarization. The polarization of M2 macrophages transduced by the ASIC3-M-CSF signal promotes the differentiation of fibroblasts into myofibroblasts through transforming growth factor β1 (TGF-β1), thereby producing ASIC3-M-CSF-TGF-β1 positive feedback loop. Targeting ASIC3 may be a new treatment strategy for skin fibrosis.

2021-10-30 | GSE186739 | GEO

A runaway PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma (ChIP-seq)

Project description:PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma

2018-12-28 | GSE124430 | GEO

A runaway PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma (RNA-Seq)

Project description:PRH/HHEX-Notch3 feedback loop drives cholangiocarcinoma

2018-12-28 | GSE124429 | GEO

Epigenetic regulation of iASPP-p63 feedback loop in cutaneous squamous cell carcinoma

Project description:Keratinocyte skin cancer, comprising cutaneous squamous (cSCC) and basal cell carcinoma, is the most common malignancy in the UK. P53 is frequently mutated in cSCC. iASPP is a key inhibitor of p53 and NF-kB signalling pathways and has been documented as highly expressed in several types of human cancer. We have previously identified an autoregulatory feedback loop between iASPP and p63, which is critical in epidermal homeostasis. We hypothesised a potential role for dysregulation of this axis in the pathogenesis of keratinocyte malignancies. Immunostaining of 116 cSCC clinical samples revealed increased iASPP and ΔNp63 expression but also highlighted a significant alteration of iASPP cellular localisation, with consequent deregulation of its function. Expression patterns, functionality, gene and microRNA expression analysis were further investigated in 10 cSCC cell lines. Our data suggest that whilst direct effects of iASPP and p63 upon each other’s expression are maintained in cSCC, epigenetic dysregulation of the feedback loop occurs at the microRNA level by a novel mechanism controlling p63 expression. We demonstrate that this autoregulatory feedback loop controls cell migration in cSCC by blocking EMT and promoting proliferation, and provides future directions for clinical biomarker and therapeutic target discovery in cutaneous SCC.

2019-11-20 | GSE123189 | GEO

Analyses of RNAi-heterochromatin positive feedback loop in Tetrahymena

Project description:Analyses of RNAi-heterochromatin positive feedback loop in Tetrahymena

| PRJNA343227 | ENA

An autoregulatory feedback loop converging on H2AK119ub1 drives synovial sarcoma

Project description:An autoregulatory feedback loop converging on H2AK119ub1 drives synovial sarcoma

| PRJNA848404 | ENA

Analyses of scnRNAs in the mutatnts defective in an RNAi-heterochromatin positive feedback loop in Tetrahymena [scnRNA]

Project description:In the ciliated protozoan Tetrahymena, an RNAi-mediated feedback loop is important for assembling heterochromatin on the sequences that are removed from the somatic genome by programmed DNA elimination. Because heterochromatin is formed exclusively on the eliminated sequences, some mechanism must inhibit this feedback loop at the boundaries of the eliminated sequences. In this study, we show that the HP1-like protein Coi6p, its interaction partners Coi7p and Lia5p, and the histone demethylase Jmj1p are crucial for confining the production of small RNAs to the eliminated sequences.

2017-03-06 | GSE87011 | GEO

Dicer and Hsp104 function in a negative feedback loop to confer epigenetic robustness [RNA_correlations]

Project description:Epigenetic mechanisms can be influenced by environmental cues and thus evoke phenotypic variation. This plasticity can be advantageous for adaption, but also detrimental if not under tight control. Although having attracted considerable interest, it remains largely unknown if and how environmental cues such as temperature trigger epigenetic alterations. Using fission yeast, we demonstrate that environmentally induced discontinuous phenotypic variation is buffered by a negative feedback loop that involves the RNase Dicer and the protein disaggregase Hsp104. In the absence of Hsp104, Dicer accumulates in cytoplasmic inclusions and heterochromatin becomes unstable at elevated temperatures, an epigenetic state that is inherited for many generations after the heat stress. Dicer instead averts the toxic aggregation of a prionogenic protein. Our results highlight the importance of feedback regulation in building epigenetic memory and uncover Hsp104 and Dicer as homeostatic controllers that buffer environmentally induced stochastic epigenetic variation and toxic aggregation of prionogenic proteins. Various strains grown at 30°C or 37°C

2015-04-23 | E-GEOD-60638 | biostudies-arrayexpress

Dicer and Hsp104 function in a negative feedback loop to confer epigenetic robustness [RNA_profiles]

2015-04-23 | E-GEOD-60429 | biostudies-arrayexpress

Analyses of heterochromatin distributions in the mutatnts defective in an RNAi-heterochromatin positive feedback loop in Tetrahymena [ChIP]

Project description:In the ciliated protozoan Tetrahymena, an RNAi-mediated feedback loop is important for assembling heterochromatin on the sequences that are removed from the somatic genome by programmed DNA elimination. Because heterochromatin is formed exclusively on the eliminated sequences, some mechanism must inhibit this feedback loop at the boundaries of the eliminated sequences. In this study, we show that the HP1-like protein Coi6p, its interaction partners Coi7p and Lia5p, and the histone demethylase Jmj1p are crucial for confining the formation of heterochromatin to the eliminated sequences.

2017-03-06 | GSE87013 | GEO

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