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Melatonin inhibits fibroblast cell functions and hypertrophic scar formation by enhancing autophagy through the MT2 receptor-inhibited PI3K/Akt /mTOR signaling

ABSTRACT: Melatonin inhibits fibroblast cell functions and hypertrophic scar formation by enhancing autophagy through the MT2 receptor-inhibited PI3K/Akt /mTOR signaling

PROVIDER: PRJNA785978 | ENA |

REPOSITORIES: ENA

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Melatonin inhibits fibroblast cell functions and hypertrophic scar formation by enhancing autophagy through the MT2 receptor-inhibited PI3K/Akt /mTOR signaling

Project description:Hypertrophic scar (HS) is a fibrotic skin condition and characterized by abnormal proliferation of myofibroblasts and accumulation of extracellular matrix. Melatonin, an endogenous hormone, can alleviate fibrosis in multiple models of diseases. This study examined the effect of melatonin on fibrosis in primary fibroblasts from human HS (HSFs) and a rabbit ear model and potential mechanisms. Melatonin treatment significantly decreased the migration and contraction capacity, collagen and α-smooth muscle actin (α-SMA) production in HSFs. RNA-sequencing and bioinformatic analyses indicated that melatonin modulated the expression of genes involved in autophagy and oxidative stress. Mechanistically, melatonin treatment attenuated the AKT/mTOR activation through affecting the binding of MT2 receptor with PI3K to enhance autophagy, decreasing fibrogenic factor production in HSFs. Moreover, melatonin treatment inhibited HS formation in rabbit ears by enhancing autophagy. The anti-fibrotic effects of melatonin were abrogated by treatment with an autophagy inhibitor (3-methyladenine, 3-MA), an Akt activator (SC79), or an MT2 selective antagonist (4-phenyl-2propionamidotetralin, 4-P-PDOT). Therefore, melatonin may be a potential drug for prevention and treatment of HS.

2022-06-03 | GSE190135 | GEO

Epigenome analysis of normal skin and hypertrophic scar samples

Project description:Hypertrophic scarring (HS) is characterized by excessive extracellular matrix deposition, matrix metalloprotein gene activation, and fibroblast invasive growth. However, the methylation level of hypertrophic scarring is poorly understood. Genome wide DNA methylation profiling of normal skin and hypertrophic scar. The Illumina Infinium Methylation EPIC BeadChip (850K) was used to obtain DNA methylation profiles across approximately 853,307 CpGs in liquid based scar samples. Samples included 6 normal skin, and 6 hypertrophic scar.

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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

RNA-seq of human hypertrophic scar fibroblast cell treated with fkbp10 siRNA against untreated controls

Project description:human hypertrophic scar fibroblast cell treated with fkbp10 siRNA and control siRNA for 48 hours

2020-08-26 | E-MTAB-9471 | biostudies-arrayexpress

RNA-seq of human hypertrophic scar fibroblast cell treated with pcolce siRNA against untreated controls

Project description:human hypertrophic scar fibroblast cell treated with pcolce siRNA and control siRNA for 48 hours

2020-08-26 | E-MTAB-9472 | biostudies-arrayexpress

The genomic response of human granulosa cells (KGN) to melatonin and specific agonists/antagonists to the melatonin receptors

Project description:Melatonin is a known modulator of follicle development, it acts through several molecular cascades via binding to its two high-affinity, G-protein coupled receptors MT1 and MT2. Even though it is believed that melatonin can modulate granulosa cell (GC) functions, there is still limited knowledge of how it can act in human GC through MT1 and MT2 and which one is the major receptor implicated in the effects of melatonin on the metabolic processes in the dominant follicle. To better characterize the roles of the MT1 and MT2 receptors on the effects of melatonin on follicular atresia and the regulation of proliferation and differentiation of granulosa cells during the antral stage, human granulosa-like tumor cells (KGN) were treated with specific melatonin receptor agonists and antagonists, and gene expression was analyzed with RNA-seq technology. Following appropriate normalization and the application of a fold change cut-off of 1.5 (FC 1.5, p ≤ 0.05) for each treatment, lists of the principal differentially expressed genes (DEGs) are generated. Analysis of major upstream regulators suggested that the MT1 receptor may be involved in the melatonin antiproliferative effect by reprogramming the metabolism of human GC by activating the PKB signaling pathway. Our data suggest that melatonin may act complementary through both MT1 and MT2 receptors to modulate human GC steroidogenesis, proliferation, and differentiation. However, MT2 receptors may be the ones implicated in transducing the effects of melatonin on the prevention of GC luteinization and follicle atresia at the antral follicular stage through stimulating the PKA pathway.

2022-10-26 | GSE201943 | GEO

Lactylome and Proteome of Human Hypertrophic Scar Tissues

Project description:Here, using a label-free quantification approach, global lactylome and proteome analyses were performed based on 4 hypertrophic scar and 4 adjacent normal skin samples.

2023-11-08 | PXD046800 | iProX

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

The CD90+CD39+ and CD90+CD39- fibroblast subtypes in human hypertrophic scar and normal skin

Project description:To explore the functional difference between CD90+CD39+ and CD90+CD39- fibroblasts in human hypertrophic scar and normal skin, the gene expresson microarray was performed on Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39+ and Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39- cells sorted from suspension disgested from three human hypertrophic scar samples; and Live CD49f- E-Cadherin- Lin- CD45- CD31- CD90+ CD39+ cells sorted from suspension disgested from three human normal skin samples

2021-07-05 | GSE158766 | GEO

Pentoxifylline-induced differentially-expressed genes in hypertrophic scar fibroblasts

Project description:Pentoxifylline-induced differentially-expressed genes in hypertrophic scar fibroblasts

| PRJNA506825 | ENA