ArticleMolecular and cellular biochemistry2016
MicroRNA-143-3p inhibits hyperplastic scar formation by targeting connective tissue growth factor CTGF/CCN2 via the Akt/mTOR pathway.
Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 65 citations in OpenAlex.
- Epigenetic orchestration of scar formation: Therapeutic potential of targeting DNA methylation and non‑coding RNAs in cutaneous fibrosis (Review).Molecular medicine reports · 2026Review
- Vitamin D promotes autophagy to inhibit LPS-induced lung injury via targeting cathepsin D.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- The PI3K/AKT/mTOR pathway in scar remodeling and keloid formation: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2025Review
- Targeting MetaLnc9/miR-143/FSCN1 axis inhibits oxidative stress and myofibroblast transdifferentiation in oral submucous fibrosis.Journal of dental sciences · 2024Article
- MiR-143-3p/FNDC5 axis: a novel regulator of insulin sensitivity.Endocrine · 2024Article
- Deciphering Collagen Phenotype Dynamics Regulators: Insights from In-Silico Analysis.Journal of bioinformatics and systems biology : Open access · 2024Article
- Mechanisms underlying pathological scarring by fibroblasts during wound healing.International wound journal · 2023Article
- Expression of microRNAs in leukocytes and serum of asbestosis patients.European journal of medical research · 2023Article
- [Research advances on the role and mechanism of microRNA in hypertrophic scar].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Article
- Beyond the Code: Noncoding RNAs in Skin Wound Healing.Cold Spring Harbor perspectives in biology · 2022Article
- Clinical Efficacy and Safety of Pulsed Dye Laser Combined with Pingyangmycin on Hyperplastic Scar after Acne.Mediators of inflammation · 2022Article
- Identifying miRNAs Associated with the Progression of Keloid through mRNA-miRNA Network Analysis and Validating the Targets of miR-29a-3p in Keloid Fibroblasts.BioMed research international · 2022Article
- Article
- 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
- Elucidation of the Hdac2/Sp1/Molecular therapy. Nucleic acids · 2021Article
- CCN2 (Cellular Communication Network factor 2) in the bone marrow microenvironment, normal and malignant hematopoiesis.Journal of cell communication and signaling · 2021Review
- MiR-3613-3p inhibits hypertrophic scar formation by down-regulating arginine and glutamate-rich 1.Molecular and cellular biochemistry · 2021Article
- Preliminary construction of a regulatory network of miRNAs in the pathogenesis of nucleus pulposus degeneration - a review based on data mining.American journal of translational research · 2021Review
- LncRNA OIP5‑AS1 aggravates house dust mite‑induced inflammatory responses in human bronchial epithelial cells via the miR‑143‑3p/HMGB1 axis.Molecular medicine reports · 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
Post-traumatic hypertrophic scar (HS) is a fibrotic disease with excessive extracellular matrix (ECM) production, which is a response to tissue injury by fibroblasts. Although emerging evidence has indicated that miRNA contributes to hypertrophic scarring, the role of miRNA in HS formation remains unclear. In this study, we found that miR-143-3p was markedly downregulated in HS tissues and fibroblasts (HSFs) using qRT-PCR. The expression of connective tissue growth factor (CTGF/CCN2) was upregulated both in HS tissues and HSFs, which is proposed to play a key role in ECM deposition in HS. The protein expression of collagen I (Col I), collagen III (Col III), and α-smooth muscle actin (α-SMA) was obviously inhibited after treatment with miR-143-3p in HSFs. The CCK-8 assay showed that miR-143-3p transfection reduced the proliferation ability of HSFs, and flow cytometry showed that either early or late apoptosis of HSFs was upregulated by miR-143-3p. In addition, the activity of caspase 3 and caspase 9 was increased after miR-143-3p transfection. On the contrary, the miR-143-3p inhibitor was demonstrated to increase cell proliferation and inhibit apoptosis of HSFs. Moreover, miR-143-3p targeted the 3'-UTR of CTGF and caused a significant decrease of CTGF. Western blot demonstrated that Akt/mTOR phosphorylation and the expression of CTGF, Col I, Col III, and α-SMA were inhibited by miR-143-3p, but increased by CTGF overexpression. In conclusion, we found that miR-143-3p inhibits hypertrophic scarring by regulating the proliferation and apoptosis of human HSFs, inhibiting ECM production-associated protein expression by targeting CTGF, and restraining the Akt/mTOR pathway.
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