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METTL3 Facilitates Hypertrophic Scar Fibrosis by Promoting pri-miRNA-31 Maturation and ZBTB20 Silencing in m6A-dependent Manner [MeRIP-Seq]

ABSTRACT: To clarify the role of METTL3-mediated m6A modification in hypertrophic scars (HS), we conditionally knocked out the m6A methyltransferase METTL3 in HS-derived dermal fibroblasts (HSFBs). We then performed MeRIP-seq analysis on HSFBs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE246978 | GEO | 2024/08/30

REPOSITORIES: GEO

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METTL3 Facilitates Hypertrophic Scar Fibrosis by Promoting pri-miRNA-31 Maturation and ZBTB20 Silencing in m6A-dependent Manner [RNA-Seq]

Project description:To clarify the role of METTL3-mediated m6A modification in hypertrophic scars (HS), we conditionally knocked out the m6A methyltransferase METTL3 in HS-derived dermal fibroblasts (HSFBs). We then performed RNA-seq analysis on normal control and Mettl3 knockdown HSFBs.

2024-08-30 | GSE246977 | GEO

The m6A RNA modification modulates gene expression and fibrosis-related pathways in hypertrophic scar

Project description:Purpose: To systematically analyze the overall m6A modification pattern in hyperplastic scars (HS). Methods: The m6A modification patterns in HS and normal skin (NS) tissues were described by m6A sequencing and RNA sequencing, and subsequently bioinformatics analysis was performed. The m6A-related RNA was immunoprecipitated and verified by real-time quantitative PCR. Results: The appearance of 14,791 new m6A peaks in the HS sample was accompanied by the disappearance of 7,835 peaks. The unique m6A-related genes in HS were thus associated with fibrosis-related pathways. We identified the differentially expressed mRNA transcripts in HS samples with hyper-methylated or hypo-methylated m6A peaks. Conclusion: This study is the first to map the m6A transcriptome of human HS, which may help clarify the possible mechanism of m6A-mediated gene expression regulation.

2021-08-08 | GSE181540 | GEO

The m6A RNA modification modulates gene expression and fibrosis-related pathways in hypertrophic scar [m6A-seq]

2022-01-24 | GSE194121 | GEO

METTL3 Facilitates Hypertrophic Scar Fibrosis by Promoting pri-miRNA-31 Maturation and ZBTB20 Silencing in m6A-dependent Manner

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-08-30 | GSE246979 | GEO

Glucocorticoid promotes fatty acids metabolism in hypertrophic scar tissues and fibroblasts via the microRNA

Project description:Hypertrophic scar (HS) is a skin lesion due to abnormal wound healing after skin injury; histologically, HS is characterized by deposition of excessive amounts of the extracellular matrix and collagen produced by wound healing-induced proliferative fibroblasts. Clinically, HS management includes surgical resection of HS, topical glucocorticoid therapy or drug injections, pressure therapy, fractional carbon dioxide laser therapy, and cryotherapy. In terms of non-surgical therapy, glucocorticoids (like Triamcinolone acetonide, a synthetic corticosteroid medication used topically to treat various skin conditions) was able to effectively inhibit HS formation safely for decades. The effects of glucocorticoids may either be due to its anti-inflammatory, anti-allergenic and immunomodulatory effects or activate fatty acids metabolism by promotion of lipid accumulation in fibroblasts. However, it is no clear why and how glucocorticoids-upregulated fatty acid metabolisms benefit in HS treatment and prevention.And it remains to be defined how altered microRNAs regulated-fatty acid metabolism involved in pathological scars.

2023-02-25 | GSE225646 | GEO

Pentoxifylline-induced differentially-expressed genes in hypertrophic scar fibroblasts

Project description:Pentoxifylline attenuated hypertrophic scars by influencing the cell cycles

2019-07-09 | GSE122891 | GEO

Gene Expression in Three Early Human Hypertrophic Scar Samples

Project description:The goal was to obtain expression data from the deep cones in early human hypertrophic scars to be used to confirm expression data obtained in a porcine model. Three samples of early human hypertrophic scar were obtained and processed with the Affymetrix Human GeneChip® Human Genome U133 plus 2.0. Sample demographics were Black 2, White 1; upper extremity 2, neck 1; times since injury 6.7 months and 10.8 months; and patient ages were 19 and 54.

2011-12-31 | E-GEOD-26213 | biostudies-arrayexpress

Gene Expression in Three Early Human Hypertrophic Scar Samples

Project description:The goal was to obtain expression data from the deep cones in early human hypertrophic scars to be used to confirm expression data obtained in a porcine model.

2011-12-31 | GSE26213 | GEO

TBK1-METTL3 axis facilitates antiviral immunity [MeRIP-seq]

Project description:mRNA m6A modification is involved in regulation of immune system. However, its function in antiviral immunity is controversial, and how immune responses regulate m6A modification is unknown. We here found TBK1, a key kinase of antiviral pathways, phosphorylated the core m6A methyltransferase METTL3 at Serine 67. The phosphorylated METTL3 interacted with translational complex and enhanced proteins translation, including IRF3, and facilitated antiviral responses. TBK1 also promoted METTL3 activation and m6A modification, which is required for stabilizing IRF3 mRNA. Type I IFN induction was severely impaired in METTL3 deficient cells. Mettl3flfl-lyz2-Cre mice were significantly more susceptible to IAV-induced lethality than control mice. Consistently, Ythdf1—/— mice cannot control viral infection and showed higher mortality than control mice due to decreased IRF3 expression. Together, we demonstrated that innate signals activated METTL3 via TBK1, and METTL3 and m6A modification secured antiviral immunity by promoting mRNA stability and protein translation.

2020-11-04 | GSE160790 | GEO

Microarray profiling analysis of microRNAs expression in Hypertrophic scar

Project description:Excessive repair after burn or trauma will lead to the formation of pathological scar. TGF-β1 is a powerful growth factor after wound healing. It is considered to be a key regulator of HS and various fibrotic diseases. MicroRNAs (miRNAs) can widely participate in the pathophysiological processes of various diseases by participating in post transcriptional gene regulation. At present, there is no research report on miR-361 and hypertrophic scar. This study found that miR-361 in HS is down-regulated. MiR-361 can inhibit the proliferation of HS fibroblasts and promote their apoptosis by inhibiting TGF-β1. Moreover, miR-361 can inhibit the formation of rabbit ear scar by inhibiting the expression of TGF-β1.

2021-11-22 | GSE189134 | GEO

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