کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8296992 | 1536773 | 2014 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Tight junction protein claudin-4 is modulated via ÎNp63 in human keratinocytes
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موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
In the epidermis, tight junction (TJ) structure is specifically located in the stratum granulosum, where the expression of ÎNp63, a p53 family transcription factor, is attenuated. Since the relationship between ÎNp63 and barrier function has not been fully uncovered, we assessed expression profiles of TJ proteins in skin tissues and cultured keratinocytes. The results showed that expression of ÎNp63 and that of claudin-4 were inversely correlated in healthy human epidermis. In vitro studies using HaCaT keratinocytes revealed functional relevance of ÎNp63 and claudin-4. Curiously, Toll-like receptor (TLR)-3 ligand, which is known to be liberated from damaged cells, suppressed ÎNp63 expression and concomitantly upregulated claudin-4 expression in primary keratinocytes. More interestingly, a broad expression pattern of claudin-4 was found in the epidermis of atopic dermatitis (AD), a barrier defect disorder, which contains ÎNp63-lacking keratinocytes as we reported previously. Therefore, upregulation of claudin-4 expression regulated by ÎNp63 might be associated with complementary or repair responses of damaged keratinocytes with AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 455, Issues 3â4, 12 December 2014, Pages 205-211
Journal: Biochemical and Biophysical Research Communications - Volume 455, Issues 3â4, 12 December 2014, Pages 205-211
نویسندگان
Terufumi Kubo, Kotaro Sugimoto, Takashi Kojima, Norimasa Sawada, Noriyuki Sato, Shingo Ichimiya,