کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5649465 | 1407125 | 2016 | 33 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TSLP Down-Regulates S100A7 and Ã-Defensin 2 Via the JAK2/STAT3-Dependent Mechanism
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کلمات کلیدی
STAT3AMPRT-PCRhBD2T helperTSLPNHEKshuman β-defensin 2Small interfering RNA - RNA تداخل کوچکreverse transcriptase-PCR - RT-PCR معکوسsiRNA - siRNAAtopic dermatitis - درماتیت آتوپیکThymic stromal lymphopoietin - لنفوپیتین استروما تیمیکsignal transducer and activator of transcription 3 - مبدل سیگنال و فعال کننده رونویسی 3Antimicrobial peptide - پپتیدهای ضدمیکروبیnormal human epidermal keratinocytes - کراتینوسیت های اپیدرمی طبیعی انسان
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Elevated T-helper type 2 cytokines in atopic skin, such as IL-4 and IL-13, were thought to be responsible for an impaired expression of antimicrobial proteins, which may contribute to the increased susceptibility to skin infections in patients with atopic dermatitis. In this study, the relationship between thymic stromal lymphopoietin and antimicrobial proteins and the involved molecular pathway was defined in normal human epidermal keratinocytes and human skin equivalent model. Stimulation of normal human epidermal keratinocytes with thymic stromal lymphopoietin decreased both mRNA and levels of S100A7 and human β-defensin 2 in a dose-dependent manner, and the regulation was JAK2/STAT3-dependent. Thymic stromal lymphopoietin decreased the antimicrobial protein expression, even in the presence of IL-17, which is their strong inducer. STAT3 directly regulated the S100A7 and human β-defensin 2 promoters in normal human epidermal keratinocytes. Immunohistochemically, lesional atopic skin stained more intensely with phospho-STAT3 compared with healthy control. Our results show that up-regulated thymic stromal lymphopoietin may contribute to the deficiency of antimicrobial proteins in atopic dermatitis, including S100A7 and human β-defensin 2, by a JAK2/STAT3-dependent mechanism and that STAT3/Sin3a might directly control the transcriptional activity of the antimicrobial protein promoters in normal human epidermal keratinocytes. Taken together, a key role of the JAK2/STAT3/Sin3a signaling pathway in thymic stromal lymphopoietin-mediated immune response in normal human epidermal keratinocytes might give us clues to understanding the pathological signal transductions in atopic dermatitis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 136, Issue 12, December 2016, Pages 2427-2435
Journal: Journal of Investigative Dermatology - Volume 136, Issue 12, December 2016, Pages 2427-2435
نویسندگان
Hana Lee, Woo-In Ryu, Hee Joo Kim, Hyun Cheol Bae, Hwa Jung Ryu, Jung Jin Shin, Kwon-Ho Song, Tae Woo Kim, Sang Wook Son,