ArticleMolecular medicine reports2017
MicroRNA‑185 regulates transforming growth factor‑β1 and collagen‑1 in hypertrophic scar fibroblasts.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Exosomes and microRNAs: insights into their roles in thermal-induced skin injury, wound healing and scarring.Molecular genetics and genomics : MGG · 2024Review
- Lipoaspirate fluid derived factors and extracellular vesicles accelerate wound healing in a rat burn model.Frontiers in bioengineering and biotechnology · 2023Article
- Innovative Treatment Strategies to Accelerate Wound Healing: Trajectory and Recent Advancements.Cells · 2022Review
- MicroRNA Alterations Induced in Human Skin by Diesel Fumes, Ozone, and UV Radiation.Journal of personalized medicine · 2022Article
- Targeting microRNA for improved skin health.Health science reports · 2021Review
- USP15 Enhances the Proliferation, Migration, and Collagen Deposition of Hypertrophic Scar-Derived Fibroblasts by Deubiquitinating TGF-βR1 In Vitro.Plastic and reconstructive surgery · 2021Observational
- Hypertrophic Scarring: Current Knowledge of Predisposing Factors, Cellular and Molecular Mechanisms.Journal of burn care & research : official publication of the American Burn Association · 2020Review
- tRNA‑derived small RNAs: A novel class of small RNAs in human hypertrophic scar fibroblasts.International journal of molecular medicine · 2020Article
- MicroRNA-494 targets PTEN and suppresses PI3K/AKT pathway to alleviate hypertrophic scar formation.Journal of molecular histology · 2019Article
- Article
- MicroRNA-205-5p regulates extracellular matrix production in hyperplastic scars by targeting Smad2.Experimental and therapeutic medicine · 2019Article
- Reactive Oxygen Species Drive Epigenetic Changes in Radiation-Induced Fibrosis.Oxidative medicine and cellular longevity · 2019Review
- miR-185 and miR-29a are similarly expressed in the bronchoalveolar lavage cells in IPF and lung cancer but common targets DNMT1 and COL1A1 show disease specific patterns.Molecular medicine reports · 2018Article
- miR-185 Inhibits Fibrogenic Activation of Hepatic Stellate Cells and Prevents Liver Fibrosis.Molecular therapy. Nucleic acids · 2018Article
- Role of MicroRNA in Proliferation Phase of Wound Healing.Frontiers in genetics · 2018Review
- Molecular Pathogenesis of Chlamydia Disease Complications: Epithelial-Mesenchymal Transition and Fibrosis.Infection and immunity · 2018Article
- Suppressive effects of human fetal keratinocytes on the proliferation, differentiation and extracellular matrix synthesis of human hypertrophic scar fibroblasts in vitro.Molecular medicine reports · 2017Article
- MicroRNA-98 inhibits the cell proliferation of human hypertrophic scar fibroblasts via targeting Col1A1.Biological research · 2017Article
- Blockade of LINC01605-enriched exosome generation in M2 macrophages impairs M2 macrophage-induced proliferation, migration, and invasion of human dermal fibroblasts.International journal of immunopathology and pharmacologyArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β1 (TGF-β1) and collagen type I (Col-1) serve a critical role in the development and progression of hypertrophic scarring (HS). The present study hypothesized that a post‑translational mechanism of microRNAs (miR) regulated the expression of TGF‑β1 and Col‑1 in HS fibroblasts (HSFBs). A collection of 20 HS tissues was compared with corresponding normal tissues from clinical patients, and the expression of miR‑185 was measured. Using PicTar, TargetScan and miRBase databases, it was identified that miR‑185 may be a regulator of TGF‑β1 and Col‑1 in humans. Based on these hypotheses, the expression of miR‑185, TGF‑β1 and Col‑1 in HS tissues was investigated. The results demonstrated that the expression of miR‑185 was markedly suppressed, and TGF‑β1 and Col‑1 levels were increased, in HS tissues. The expression levels of endogenous miR‑185 negatively correlated with the TGF‑β1 and Col‑1 mRNA levels (Pearson's correlation coefficient r=‑0.674, P<0.01 and r=‑0.590, P<0.01, respectively). In vitro, miR‑185 can regulate TGF‑β1 and Col‑1 through the predicted binding sites in its 3'‑untranslated region. miR‑185 had an effect on cell proliferation and apoptosis, thereby regulating HSFBs growth. In addition, miR‑185 gain‑of‑function decreased TGF‑β1 and Col‑1 protein expression, and miR‑185 loss‑of‑function increased TGF‑β1 and Col‑1 protein expression in HSFBs. In conclusion, overexpressed miR‑185 could inhibit HSFBs growth, and the underlying mechanism was mediated, at least partly, through the suppression of TGF‑β1 and Col‑1 expression. However, above all, miR‑185 might serve as a potential therapeutic approach for the treatment of HS.
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