کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6076519 1203518 2014 10 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Original ArticleReversal of Murine Epidermal Atrophy by Topical Modulation of Calcium Signaling
ترجمه فارسی عنوان
مقاله اصلی در مورد آتروفی اپیدرمی موش توسط مدولاسیون موضعی سیگنالینگ کلسیم
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی امراض پوستی
چکیده انگلیسی

Cytosolic Ca2+ signals are performed by Ca2+ releases from the endoplasmic reticulum and Ca2+ influx from the extracellular medium. Releases rely on the refilling of the intracellular Ca2+ stores by the Ca2+ influx “Store-Operated Calcium Entry” (SOCE) via the channel Orai1. Here we show that Orai1 expression, SOCE amplitude, and epidermal proliferation are decreased in the epidermis of patients with skin fragility when compared with aged nonatrophic skin. Epidermal atrophy was induced in mice by the inhibition of Orai1 with small interfering RNA and the topical application of a SOCE blocker BTP2. The inhibition of Orai1 impaired the heparin-binding epidermal growth factor (HB-EGF)-induced Ca2+ influxes and fully prevented the mitogen effect of HB-EGF in primary human keratinocytes. Importantly, epidermal proliferation correlated with Orai1 expression in mice. Conversely, the topical application of an Orai1 activator, the benzohydroquinone (BHQ), increased the epidermal thickness and proliferation, whereas the pro-proliferative effect of BHQ was prevented by the inhibition of Orai1. Finally, the topical application of BHQ reversed the epidermal atrophy induced by corticosteroids in mice. The topical modulation of Ca2+ signals may thus be a promising therapeutic strategy in dermatology.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 134, Issue 6, June 2014, Pages 1599-1608
نویسندگان
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