دورية أكاديمية

S100A12 Induced in the Epidermis by Reduced Hydration Activates Dermal Fibroblasts and Causes Dermal Fibrosis.

التفاصيل البيبلوغرافية
العنوان: S100A12 Induced in the Epidermis by Reduced Hydration Activates Dermal Fibroblasts and Causes Dermal Fibrosis.
المؤلفون: Zhao J; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA; Department of Burns, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China., Zhong A; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA; Department of Plastic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China., Friedrich EE; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA., Jia S; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA., Xie P; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA., Galiano RD; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA., Mustoe TA; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA., Hong SJ; Laboratory for Wound Repair and Regenerative Surgery, Department of Surgery/Plastic Surgery Division, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, USA. Electronic address: seok-hong@northwestern.edu.
المصدر: The Journal of investigative dermatology [J Invest Dermatol] 2017 Mar; Vol. 137 (3), pp. 650-659. Date of Electronic Publication: 2016 Nov 10.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 0426720 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1523-1747 (Electronic) Linking ISSN: 0022202X NLM ISO Abbreviation: J Invest Dermatol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2016- : New York : Elsevier
Original Publication: Baltimore, Williams & Wilkins.
مواضيع طبية MeSH: Epidermis/*metabolism , Epidermis/*pathology , Fibroblasts/*metabolism , S100A12 Protein/*metabolism, Animals ; Cell Culture Techniques ; Cell Line, Tumor ; Cicatrix, Hypertrophic/metabolism ; Coculture Techniques ; Culture Media, Conditioned ; Female ; Fibrosis ; Humans ; Inflammation ; Keloid/metabolism ; Keratinocytes/cytology ; RNA Interference ; Rabbits ; Receptor for Advanced Glycation End Products/metabolism ; Toll-Like Receptor 4/metabolism
مستخلص: Disruption of the barrier function of skin increases transepidermal water loss and up-regulates inflammatory pathways in the epidermis. Consequently, sustained expression of proinflammatory cytokines from the epidermis is associated with dermal scarring. We found increased expression of S100A12 in the epidermis of human hypertrophic and keloid scar. Exposing a stratified keratinocyte culture to a reduced-hydration environment increased the expression and secretion of S100A12 by nearly 70%, which in turn activated dermal fibroblasts in vitro. Direct treatment of fibroblasts with conditioned medium collected from stratified keratinocyte culture under reduced-hydration conditions activated fibroblasts, shown by up-regulation of α-smooth muscle actin, pro-collagen 1, and F-actin expression. However, this fibroblast activation was not found when S100A12 was knocked down by RNA interference in keratinocytes. Pharmacological blockade of S100A12 receptors, RAGE, or TLR4 inhibited S100A12-induced fibroblast activation. Local delivery of S100A12 resulted in a marked hypertrophic scar formation in a validated rabbit hypertrophic scar model compared with saline control. Our findings indicate that S100A12 functions as a proinflammatory cytokine and suggest that S100A12 is a potential therapeutic target for dermal scarring.
(Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)
المشرفين على المادة: 0 (AGER protein, human)
0 (Culture Media, Conditioned)
0 (Receptor for Advanced Glycation End Products)
0 (S100A12 Protein)
0 (S100A12 protein, human)
0 (TLR4 protein, human)
0 (Toll-Like Receptor 4)
تواريخ الأحداث: Date Created: 20161115 Date Completed: 20170726 Latest Revision: 20220331
رمز التحديث: 20221213
DOI: 10.1016/j.jid.2016.10.040
PMID: 27840235
قاعدة البيانات: MEDLINE
الوصف
تدمد:1523-1747
DOI:10.1016/j.jid.2016.10.040