MiR-3613-3p inhibits hypertrophic scar formation by down-regulating arginine and glutamate-rich 1

Li, Lisha; Han, Weiqiang; Chen, Yun; Chen, Yuhua

doi:10.1007/s11010-020-03968-4

Cited by 12 publications

(7 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…10,[59][60][61][62] showed promising effectiveness of anti-fibrosis and remodeling on alleviating scar formation and accelerated wound healing. Li et al 63 demonstrated that miR-3613-3p inhibited HS formation via targeting arginine and glutamate-rich 1, which may provide potential therapeutic targets for the management of HS. Zhang et al 64 verified that miR-124-3p could inhibit the proliferation of HS fibroblasts by targeting TGF-β1 and may thus be a potential therapeutic target for HS.…”

Section: Discussionmentioning

confidence: 99%

Exosome Derived from Mesenchymal Stem Cells Alleviates Pathological Scars by Inhibiting the Proliferation, Migration and Protein Expression of Fibroblasts via Delivering miR-138-5p to Target SIRT1

Zhao¹,

Zhang²,

Zang³

et al. 2022

IJN

View full text Add to dashboard Cite

Introduction The therapies of using exosomes derived from mesenchymal stem cells (MSC-Exo) for wound healing and scar attenuation and micro RNAs (miRNAs) for regulation of genes by translational inhibition and mRNA destabilization obtained great achievements. Silent information regulator 1 (SIRT1) is the silent information, which has an intricate role in many biological processes. However, the effects of SIRT1 and miR-138-5p loaded in MSC-Exo on pathological scars remain unclear. Methods MSC-Exo was isolated and identified by ultracentrifugation, transmission electron microscopy, nanoparticle size measuring instrument and Western blot assays. The relationship between SIRT1 and miR-138-5p was verified by a double-luciferase reporter assay. Cell Counting Kit-8, Τranswell, scratch, and Western blot assays were used to evaluate the proliferation and migration of human skin fibroblasts (HSFs), and the protein expression of SIRT1, NF-κB, α-SMA and TGF-β1 in HSFs, respectively. Flow cytometry was used to assess the apoptosis and cell cycle of HSFs affected by SIRT1. Results Our study demonstrated that miR-138-5p loaded in MSC-Exo could attenuate proliferation, migration and protein expression of HSFs-derived NF-κB, α-SMA, and TGF-β1 by targeting to SIRT1 gene, which confirmed the potential effects of MSC-Exo in alleviating pathological scars by performing as a miRNA’s delivery vehicle. Conclusion Exosomes derived from MSCs acting as a delivery vehicle to deliver miR-138-5p can downregulate SIRT1 to inhibit the growth and protein expression of HSFs and attenuate pathological scars.

show abstract

Section: Discussionmentioning

confidence: 99%

Exosome Derived from Mesenchymal Stem Cells Alleviates Pathological Scars by Inhibiting the Proliferation, Migration and Protein Expression of Fibroblasts via Delivering miR-138-5p to Target SIRT1

Zhao¹,

Zhang²,

Zang³

et al. 2022

IJN

View full text Add to dashboard Cite

show abstract

“…MicroRNAs (miRNAs) can be competitively sponged by mRNAs as well as long non-coding RNAs (lncRNAs), and these can form competitive endogenous RNA (ceRNA) networks, which have been reported to regulate multiple biological processes to engage in the pathogenesis of many diseases including HTS [ 2 , 3 ]. For example, miR-422a has been shown to have the potential to inhibit cell proliferation in glioblastoma [ 4 ] and fibrotic genes in liver fibrosis [ 5 ]; miR-2116-3p has proven to hinder the proliferation of breast cancer cells [ 6 ]; miR-3187-3p has been reported to impede fibroblast proliferation [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Identification and functional analysis of a three-miRNA ceRNA network in hypertrophic scars

et al. 2021

View full text Add to dashboard Cite

Background Hypertrophic scar (HTS) is a fibrotic disorder of skins and may have repercussions on the appearance as well as functions of patients. Recent studies related have shown that competitive endogenous RNA (ceRNA) networks centering around miRNAs may play an influential role in HTS formation. This study aimed to construct and validate a three-miRNA (miR-422a, miR-2116-3p, and miR-3187-3p) ceRNA network, and explore its potential functions. Methods Quantitative real‑time PCR (qRT‑PCR) was used to compare expression levels of miRNAs, lncRNAs, and genes between HTS and normal skin. Target lncRNAs and genes of each miRNA were predicted using starBase as well as TargetScan database to construct a distinct ceRNA network; overlapping target lncRNAs and genes of the three miRNAs were utilized to develop a three-miRNA ceRNA network. For every network, protein–protein interaction (PPI) network analysis was performed to identify its hub genes. For each network and its hub genes, Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted to explore their possible functions. Results MiR-422a, miR-2116-3p, and miR-3187-3p were all downregulated in HTS tissues and fibroblasts. MiR-422a-based ceRNA network consisted of 101 lncRNAs with 133 genes; miR-2116-3p-centered ceRNA network comprised 85 lncRNAs and 978 genes; miR-3187-3p-derived ceRNA network encompassed 84 lncRNAs as well as 1128 genes. The three-miRNA ceRNA network included 2 lncRNAs with 9 genes, where MAPK1, FOSL2, ABI2, KPNA6, CBL, lncRNA-KCNQ1OT1, and lncRNA-EBLN3P were upregulated. According to GO and KEGG analysis, these networks were consistently related to ubiquitination. Three ubiquitination-related genes (CBL, SMURF2, and USP4) were upregulated and negatively correlated with the expression levels of the three miRNAs in HTS tissues. Conclusions This study identified a three-miRNA ceRNA network, which might take part in HTS formation and correlate with ubiquitination.

show abstract

“…Emerging evidence has indicated the vital role of miRNAs in HSFs, presenting them as a viable target in treatment for hypertrophic scarring [34][35][36][37][38]. In the present study, the lncRNA NEAT1 functioned as a competing endogenous RNA (ceRNA) to sponge miR-miR-29-3p and negatively regulate its expression.…”

Section: Discussionmentioning

confidence: 75%

Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) regulates fibroblast growth factor receptor substrate 2 (FRS2) by targeting microRNA (miR)-29-3p in hypertrophic scar fibroblasts

Chen

Tan

et al. 2021

Bioengineered

View full text Add to dashboard Cite

show abstract

MiR-3613-3p inhibits hypertrophic scar formation by down-regulating arginine and glutamate-rich 1

Cited by 12 publications

References 50 publications

Exosome Derived from Mesenchymal Stem Cells Alleviates Pathological Scars by Inhibiting the Proliferation, Migration and Protein Expression of Fibroblasts via Delivering miR-138-5p to Target SIRT1

Exosome Derived from Mesenchymal Stem Cells Alleviates Pathological Scars by Inhibiting the Proliferation, Migration and Protein Expression of Fibroblasts via Delivering miR-138-5p to Target SIRT1

Identification and functional analysis of a three-miRNA ceRNA network in hypertrophic scars

Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) regulates fibroblast growth factor receptor substrate 2 (FRS2) by targeting microRNA (miR)-29-3p in hypertrophic scar fibroblasts

Contact Info

Product

Resources

About