ArticleExperimental and therapeutic medicine2021
MicroRNA-18a-5p represses scar fibroblast proliferation and extracellular matrix deposition through regulating Smad2 expression.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Article
- Role of Transcription Factors and MicroRNAs in Regulating Fibroblast Reprogramming in Wound Healing.Journal of bioinformatics and systems biology : Open access · 2023Article
Corrections and comments
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the expression and role of microRNA-18a-5p (miR-18a-5p) during the formation of hypertrophic scar (HS), and to further explore the molecular mechanisms involved. Downregulation of miR-18a-5p in HS tissues and human HS fibroblasts (hHSFs) was detected by reverse transcription-quantitative polymerase chain reaction. The binding sites between miR-18a-5p and the 3'-untranslated region of SMAD family member 2 (Smad2) were predicted by TargetScan and confirmed by dual-luciferase reporter assay. To investigate the role of miR-18a-5p in HS formation, the effects of miR-18a-5p downregulation or upregulation on hHSFs were subsequently determined. Cell proliferation was detected by an MTT assay, while cell apoptosis was measured by flow cytometry. In addition, the protein expression levels of Smad2, Collagen I (Col I) and Col III were examined by western blot assay. The findings indicated that miR-18a-5p downregulation in hHSFs significantly promoted the cell proliferation, decreased cell apoptosis and enhanced the expression levels of Smad2, Col I and Col III protein and mRNA, whereas miR-18a-5p upregulation in hHSFs exerted opposite effects. Notably, the effects of miR-18a-5p upregulation on hHSFs were eliminated by Smad2 upregulation. In conclusion, the data indicated that miR-18a-5p was downregulated during HS formation, and its upregulation repressed scar fibroblast proliferation and extracellular matrix deposition by targeting Smad2. Therefore, miR-18a-5p may serve as a novel therapeutic target for the treatment of HS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.