The miR-93-3p/ZFP36L1/ZFX axis regulates keratinocyte proliferation and migration during skin wound healing

التفاصيل البيبلوغرافية
العنوان: The miR-93-3p/ZFP36L1/ZFX axis regulates keratinocyte proliferation and migration during skin wound healing
المؤلفون: Xiao Feng, Jincai Guo, Shuangbai Zhou, Weilin Cai
المصدر: Molecular Therapy. Nucleic Acids
Molecular Therapy: Nucleic Acids, Vol 23, Iss, Pp 450-463 (2021)
سنة النشر: 2020
مصطلحات موضوعية: 0301 basic medicine, Skin wound, miR-93-3p, Regulator, Biology, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Drug Discovery, microRNA, medicine, Gene silencing, integumentary system, lcsh:RM1-950, ZFX, Cell biology, HaCaT, lcsh:Therapeutics. Pharmacology, 030104 developmental biology, medicine.anatomical_structure, skin wound healing, 030220 oncology & carcinogenesis, ZFP36L1, Molecular Medicine, Original Article, Wound healing, Keratinocyte
الوصف: Keratinocyte proliferation and migration are crucial steps during skin wound healing. The functional role of microRNAs (miRs) remains relatively unknown during this process. miR-93 levels have been reported to increase within 24 h of skin wound healing; however, whether miR-93-3p or miR-93-5p plays a specific role in wound healing is yet to be studied. In this study, with the use of an in vivo mouse skin wound-healing model, we demonstrate that miR-93-3p is significantly upregulated, whereas there is no change in the expression of miR-93-5p during skin wound healing. In HaCaT cells, miR-93-3p overexpression increased proliferation and migration of the cells, whereas miR-93-3p inhibition had the reverse effect. Additionally, it was evident that ZFP36L1 was a direct target of miR-93-3p in keratinocytes. Further, ZFP36L1 silencing mirrored the consequences observed during miR-93-3p overexpression on both proliferation and migration of keratinocytes. In addition, we demonstrate that zinc-finger X-linked (ZFX), as a target for ZFP36L1, is involved in the promotion of the miR-93-3p/ZFP36L1 axis in keratinocyte proliferation and migration. Ultimately, we found that mouse skin wound model treatment with anti-miR-93-3p delayed wound healing. Overall, our results show that miR-93-3p is a crucial regulator of skin wound healing that facilitates keratinocyte proliferation and migration through ZFP36L1/ZFX axis.
Graphical Abstract
Feng et al. were the first to investigate the mechanism of miR-93-3p in skin wound healing. Their study demonstrated that upregulated miR-93-3p binds and downregulates ZFP36L1, causing upregulation of ZFX and subsequent stimulation of keratinocyte proliferation and migration by using a skin wound animal model and HaCaT cell line.
تدمد: 2162-2531
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d064c0869d7249f154554ae90e750b14
https://pubmed.ncbi.nlm.nih.gov/33473330
حقوق: OPEN
رقم الأكسشن: edsair.doi.dedup.....d064c0869d7249f154554ae90e750b14
قاعدة البيانات: OpenAIRE