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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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			Action	DRS
	SRR16609136_1.fastq.gz	Fastqsanger.gz
	SRR16609136_2.fastq.gz	Fastqsanger.gz
	SRR16609137_1.fastq.gz	Fastqsanger.gz
	SRR16609137_2.fastq.gz	Fastqsanger.gz
	SRR16609138_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

The ASIC3-M-CSF-M2 macrophage-positive feedback loop modulates fibroblast-to-myofibroblast differentiation 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. 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 an ASIC3-M-CSF-TGF-β1 positive feedback loop. Targeting ASIC3 may be a new treatment strategy for skin fibrosis.

| S-EPMC9167818 | biostudies-literature

Human monocyte-derived macrophages polarized by GM-CSF (M1) or M-CSF (M2) in the presence or absence of 50 nanomolar Methotrexate

Project description:Identification of genes differentially expressed between human monocyte-macrophages generated in the presence of either GM-CSF (termed M1) or M-CSF (termed M2) and in the presence (+MTX) or absence (-) of Methotrexate

2017-05-08 | GSE71253 | GEO

Human monocyte-derived macrophages polarized by GM-CSF (M1) or M-CSF (M2) in the presence or absence of 5 micromolar methotrexate

2020-12-31 | GSE64531 | 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

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

Analyses of RNAi-heterochromatin positive feedback loop in Tetrahymena

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

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p53-dependent R-loop formation and HPV pathogenesis

Project description:p53-dependent R-loop formation and HPV pathogenesis

| PRJNA1003492 | ENA

Human monocyte-derived macrophages polarized by GM-CSF or M-CSF

Project description:Identification of genes differentially expressed between human monocyte-macrophages generated in the presence of either GM-CSF (termed M1) or M-CSF (termed M2)

2012-04-13 | GSE27792 | GEO

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