國家衛生研究院 NHRI:Item 3990099045/14921
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 909962      Online Users : 792
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
    •  Adv. Search
    Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer Goto mobile version


    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/14921


    Title: Gasdermin a is required for epidermal cornification during skin barrier regeneration and in an atopic dermatitis-like model
    Authors: Huang, LY;Li, ST;Lin, SC;Kao, CH;Hong, CH;Lee, CH;Yang, LT
    Contributors: Institute of Cellular and Systems Medicine
    Abstract: Atopic dermatitis (AD) is featured with impaired skin barrier. The stratum corneum (SC) and the intercellular tight junctions (TJs) constitute the permeability barrier, which is essential to protect the host water loss and pathogen entrance. The epidermal barrier is constantly renewed by differentiating keratinocytes through cornification, during which autophagy contributes to organelles and nucleus elimination. The human GSDMA and its mouse homologs Gsdma1-3 are expressed in the suprabasal epidermis. Although a pyroptotic role for GSDMA/Gsdma1 in host defense against Streptococcus pyogenes has been reported, the physiological function of Gsdma1/a2/a3 in epidermal homeostasis remains elusive. Herein, through repeated epidermal barrier disruption, we found that TJ formation and SC maturation were defective in the Gsdma1/a3-deficient epidermis. Using comparative gene profiling analysis, mitochondrial respiration measurement, and in vivo tracing of mitophagy, our data indicate that Gsdma1/a3 activation leads to mitochondrial dysfunction and subsequently facilitates mitochondrial turnover and epidermal cornification. In calcipotriol (MC903)-induced AD-like animal model, we demonstrated that Gsdma1/a3-deficiency selectively enhanced the Th2 response. Remarkably, the GSDMA expression is reduced in the epidermis of patients with AD compared to normal individuals. Gsdma1/a3-deficiency might be involved in AD pathogenesis, likely through GSDMA-mediated epidermal differentiation and cornification.
    Date: 2023-09
    Relation: Journal of Investigative Dermatology. 2023 Sep;143(9):1735-1745.e11.
    Link to: http://dx.doi.org/10.1016/j.jid.2023.03.1657
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-202X&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:001063247800001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85153390643
    Appears in Collections:[Liang-Tung Yang] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    PUB36965577.pdf57847KbAdobe PDF171View/Open


    All items in NHRI are protected by copyright, with all rights reserved.

    Related Items in TAIR

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback