ArticleExperimental and therapeutic medicine2018
MicroRNA-663 regulates the proliferation of fibroblasts in hypertrophic scars via transforming growth factor-β1.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- Screening and Functional Analysis of tsRNAs Associated with Diabetic Foot Ulcer Tissues.Biomedicines · 2025Article
- Native Collagen for Surgical Wound and Scar Prevention-A Six-Case Clinical Series.Journal of clinical medicine · 2025Article
- [Research advances on the role and mechanism of microRNA in hypertrophic scar].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Single-Cell RNA-Sequencing Reveals the Cellular and Genetic Heterogeneity of Skin Scar to Verify the Therapeutic Effects and Mechanism of Action of Dispel-Scar Ointment in Hypertrophic Scar Inhibition.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The Role of Extracellular Matrix in Skin Wound Healing.Journal of clinical medicine · 2021Review
- [Expression and effect of microRNA-627 in human hypertrophic scar].Zhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021Article
- Strategies to prevent hypertrophic scar formation: a review of therapeutic interventions based on molecular evidence.Burns & trauma · 2020Review
- Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study determined the expression of microRNA (miR)-663 in hypertrophic scar (HS) tissues and investigate the regulatory mechanisms of miR-663 in HS. A total of 51 patients diagnosed with HS between December 2013 and February 2016 were included in the present study. HS tissues (experimental group) and HS-adjacent tissues (control group) were collected. Primary fibroblasts were obtained from HS tissue and transfected with small-interfering RNA against transforming growth factor (TGF)-β1 or miR-663 mimics. Reverse-transcription quantitative PCR was used to determine the levels of TGF-β1 mRNA and miR-663. Western blot analysis was performed to determine TGF-β1 protein expression. An MTT assay was employed to detect the proliferation of fibroblasts, and a dual luciferase reporter assay was performed to identify the binding of miR-663 with TGF-β1 mRNA. TGF-β1 was found to have a regulatory role in HS at the transcriptional level. The expression of TGF-β1 was upregulated in HS tissues, and knockdown of TGF-β1 in cultured fibroblasts led to inhibition of proliferation. The expression of miR-663 was downregulated in HS. miR-663 was revealed to regulate the expression of TGF-β1 by binding with the 3'-untranslated region of TGF-β1 mRNA. Elevated expression of miR-663 inhibited the proliferation of fibroblasts by regulating TGF-β1 expression. The present study demonstrated that upregulation of TGF-β1 in HS tissues is associated with the downregulation of miR-663 expression. miR-663 may regulate the proliferation of fibroblasts in HS and the expression of associated proteins.
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