ArticleBiological research2017
MicroRNA-98 inhibits the cell proliferation of human hypertrophic scar fibroblasts via targeting Col1A1.
Article in Biological research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Efficacy of MSC-derived small extracellular vesicles in treating type II diabetic cutaneous wounds: a systematic review and meta-analysis of animal models.Frontiers in endocrinology · 2024Pooled it
- Overexpression of miR-431-5p Inhibits the Development of Hypertrophic Scars by Negatively Regulating the Expression of ZEB1.Journal of cosmetic dermatology · 2025Article
- Elucidating the dual roles of apoptosis and necroptosis in diabetic wound healing: implications for therapeutic intervention.Burns & trauma · 2025Review
- Immune-related inflammatory gene in hypertrophic scar: prognostic and molecular mechanisms via integrated machine learning-WGCNA analysis.Frontiers in immunology · 2025Article
- Understanding molecular mechanisms and miRNA-based targets in diabetes foot ulcers.Molecular biology reports · 2024Review
- Deciphering Collagen Phenotype Dynamics Regulators: Insights from In-Silico Analysis.Journal of bioinformatics and systems biology : Open access · 2024Article
- Let-7 family regulates HaCaT cell proliferation and apoptosis via the ΔNp63/PI3K/AKT pathway.Open medicine (Warsaw, Poland) · 2024Article
- Mechanisms underlying pathological scarring by fibroblasts during wound healing.International wound journal · 2023Article
- Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023Review
- LncRNA FPASL suppresses fibroblast proliferation through its DNA methylation via DNMT3b in hypertrophic scar.Acta biochimica et biophysica Sinica · 2022Article
- Knockdown of lncRNA-NEAT1 expression inhibits hypoxia-induced scar fibroblast proliferation through regulation of the miR-488-3p/COL3A1 axis.Experimental and therapeutic medicine · 2022Article
- The Regulation of Collagen Processing by miRNAs in Disease and Possible Implications for Bone Turnover.International journal of molecular sciences · 2021Review
- Targeting microRNA for improved skin health.Health science reports · 2021Review
- Identification of potential micro-messenger RNAs (miRNA-mRNA) interaction network of osteosarcoma.Bioengineered · 2021Article
- Article
- Transdermal delivery of Chinese herbal medicine extract using dissolvable microneedles for hypertrophic scar treatment.Acta pharmaceutica Sinica. B · 2021Article
- MicroRNA-497-5p downregulation inhibits cell viability, reduces extracellular matrix deposition and induces apoptosis in human hyperplastic scar fibroblasts by regulating Smad7.Experimental and therapeutic medicine · 2021Article
- Identification of Hub Genes and Pathways Associated With Idiopathic Pulmonary FibrosisFrontiers in molecular biosciences · 2021Article
- Single-Cell and Bulk Transcriptome Data Integration Reveals Dysfunctional Cell Types and Aberrantly Expressed Genes in Hypertrophic Scar.Frontiers in genetics · 2021Article
- MicroRNA-9-5p inhibits proliferation and induces apoptosis of human hypertrophic scar fibroblasts through targeting peroxisome proliferator-activated receptor β.Biology open · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypertrophic scarring (HS) is a severe disease, and results from unusual wound healing. Col1A1 could promote the hypertrophic scar formation, and the expression of Col1A1 in HS tissue was markedly higher than that in the normal. In present study, we aimed to identify miRNAs as post-transcriptional regulators of Col1A1 in HS.
methodsMicroRNA-98 was selected as the key miRNA comprised in HS. The mRNA levels of miR-98 in HS tissues and the matched normal skin tissues were determined by qRT-PCR. MTT and flow cytometry were used to determine the influence of miR-98 on cell proliferation and apoptosis of HSFBs, respectively. Col1A1 was found to be the target gene of miR-98 using luciferase reporter assay. Luciferase assay was performed to determine the relative luciferase activity in mimic NC, miR-98 mimic, inhibitor NC and miR-98 inhibitor with Col1A13'-UTR wt or Col1A13'-UTR mt reporter plasmids. The protein expression of Col1A1 in HSFBs after transfection with mimic NC, miR-98 mimic, inhibitor NC and miR-98 inhibitor were determined by western blotting.
resultsThe mRNA level of miR-98 in HS tissues was much higher than that in the control. Transfection of HSFBs with a miR-98 mimic reduced the cell viability of HSFBs and increased the apoptosis portion of HSFBs, while inhibition of miR-98 increased cell viability and decreased apoptosis portion of HSFBs. miR-98 inhibitor increased the relative luciferase activity significantly when cotransfected with the Col1A1-UTR reporter plasmid, while the mutant reporter plasmid abolished the miR-98 inhibitor-mediated increase in luciferase activity. Western blotting revealed that overexpression of miR-98 decreased the expression of Col1A1.
conclusionsOverexpression of miR-98 repressed the proliferation of HSFBs by targeting Col1A1.
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