دورية أكاديمية
Necrostatin-1, RIP1/RIP3 inhibitor, relieves transforming growth factor β-induced wound-healing process in formation of hypertrophic scars.
| العنوان: | Necrostatin-1, RIP1/RIP3 inhibitor, relieves transforming growth factor β-induced wound-healing process in formation of hypertrophic scars. |
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| المؤلفون: | Lin PT; Department of Plastic Surgery, Gansu Provincial Hospital, Lanzhou, China., Xue XD; Department of Plastic Surgery, Gansu Provincial Hospital, Lanzhou, China., Zhao ZD; Department of Plastic Surgery, Gansu Provincial Hospital, Lanzhou, China., Lu JY; Department of Plastic Surgery, Gansu Provincial Hospital, Lanzhou, China., Xie PL; Department of Plastic Surgery, Gansu Provincial Hospital, Lanzhou, China. |
| المصدر: | Journal of cosmetic dermatology [J Cosmet Dermatol] 2021 Aug; Vol. 20 (8), pp. 2612-2618. Date of Electronic Publication: 2020 Dec 11. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: Blackwell Science Country of Publication: England NLM ID: 101130964 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1473-2165 (Electronic) Linking ISSN: 14732130 NLM ISO Abbreviation: J Cosmet Dermatol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Oxford, UK : Blackwell Science, c2002- |
| مواضيع طبية MeSH: | Cicatrix, Hypertrophic*/drug therapy , Cicatrix, Hypertrophic*/pathology, Cells, Cultured ; Fibroblasts/pathology ; Humans ; Imidazoles/pharmacology ; Indoles ; Transforming Growth Factor beta ; Transforming Growth Factor beta1 |
| مستخلص: | Background: Hypertrophic scars (HS) are common pathologic processes emerged during wound-healing process. The receptor-interacting protein kinase (RIP) might participate in keloid formation. Aims: This study aimed to investigate Necrostatin-1 (Nec-1), a RIP1/RIP3 inhibitor, in the formation of hypertrophic scar. Methods: Human hypertrophic scar fibroblasts (HSF) were extracted from patients with hypertrophic scar. Transforming growth factor-β1 (TGF-β1) was performed to induce wound-healing process including cell proliferation (CCK-8, Flow cytometry, and Western blot), migration (Transwell assay, Western blot), collagen production (Western blot), and extracellular matrix dysfunction (Western blotting and immunofluorescence). Results: Our results reported that Nec-1 inhibited TGF-β1-induced cell proliferation and promoted G0/G1 phase arrest in HSF. In addition, Nec-1 attenuated TGF-β1-induced cell migration and inhibited the expression of MMP2 and MMP9 in TGF-β1-induced HSF. Besides, Nec-1 also reduced TGF-β1-induced collagen production and α-smooth muscle actin expression in HSF. Conclusions: The present data in this study showed the potential role of Nec-1 as a novel treatment for HS. (© 2020 Wiley Periodicals LLC.) |
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| فهرسة مساهمة: | Keywords: hypertrophic scars; necrostatin-1; receptor-interacting protein kinase; transforming growth factor β; wound healing |
| المشرفين على المادة: | 0 (Imidazoles) 0 (Indoles) 0 (Transforming Growth Factor beta) 0 (Transforming Growth Factor beta1) 0 (necrostatin-1) |
| تواريخ الأحداث: | Date Created: 20201125 Date Completed: 20210806 Latest Revision: 20210806 |
| رمز التحديث: | 20240829 |
| DOI: | 10.1111/jocd.13860 |
| PMID: | 33237588 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1473-2165 |
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| DOI: | 10.1111/jocd.13860 |