کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6074813 | 1203488 | 2016 | 27 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Desmoglein 3-Dependent Signaling Regulates Keratinocyte Migration and Wound Healing
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کلمات کلیدی
GFPERKPKCp38MAPKDsg3Small interfering RNA - RNA تداخل کوچکsiRNA - siRNAdesmoglein 3 - دزوگلین 3MEK - مجاهدین خلقwild-type - نوع وحشیgreen fluorescent protein - پروتئین فلورسنت سبزProtein kinase C - پروتئین کیناز سیp38 mitogen-activated protein kinase - پروتئین کیناز متیوژن فعال p38pemphigus vulgaris - پمفیگوس ولگاریسextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
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![عکس صفحه اول مقاله: Desmoglein 3-Dependent Signaling Regulates Keratinocyte Migration and Wound Healing Desmoglein 3-Dependent Signaling Regulates Keratinocyte Migration and Wound Healing](/preview/png/6074813.png)
چکیده انگلیسی
The desmosomal transmembrane adhesion molecules desmoglein 3 (Dsg3) and desmocollin 3 (Dsc3) are required for strong keratinocyte cohesion. Recently, we have shown that Dsg3 associates with p38 mitogen-activated protein kinase (p38MAPK) and suppresses its activity. Here, we further investigated the role of Dsg3-dependent control of p38MAPK function. Dsg3-deficient mice display recurrent spontaneously healing skin erosions. In lesional and perilesional biopsies, p38MAPK activation was detectable compared with control animals. This led us to speculate that Dsg3 regulates wound repair in a p38MAPK-dependent manner. Indeed, scratch-wounded keratinocyte monolayers exhibited p38MAPK activation and loss of Dsg3 in cells lining the wound edge. Human keratinocytes after silencing of Dsg3 as well as primary cells isolated from Dsg3 knockout animals exhibited accelerated migration, which was further corroborated in an ex vivo skin outgrowth assay. Importantly, migration was efficiently blocked by inhibition of p38MAPK, indicating that p38MAPK mediates the effects observed upon loss of Dsg3. In line with this, we show that levels of active p38MAPK associated with Dsc3 are increased in Dsg3-deficient cells. These data indicate that Dsg3 controls a switch from an adhesive to a migratory keratinocyte phenotype via p38MAPK inhibition. Thus, loss of Dsg3 adhesion may foster wound closure by allowing p38MAPK-dependent migration.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 136, Issue 1, January 2016, Pages 301-310
Journal: Journal of Investigative Dermatology - Volume 136, Issue 1, January 2016, Pages 301-310
نویسندگان
Vera Rötzer, Eva Hartlieb, Julia Winkler, Elias Walter, Angela Schlipp, Miklós Sardy, Volker Spindler, Jens Waschke,