کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8716355 | 1587883 | 2017 | 41 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
6-Formylindolo[3,2-b]Carbazole Accelerates Skin Wound Healing via Activation of ERK, but Not Aryl Hydrocarbon Receptor
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کلمات کلیدی
AHRJnkERKacutely transforming retrovirus AKT8 in rodent T-cell lymphomaFICZ6-formylindolo[3,2-b]carbazoleTGF-βmitogen-activated protein kinase/extracellular signal-regulated kinasec-Jun N-terminal kinase - C-Jun N-terminal kinaseSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNAAkt - آکتtransforming growth factor-β - تبدیل فاکتور رشد βMEK - مجاهدین خلقextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیaryl hydrocarbon receptor - گیرنده آرویل هیدروکربن
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
امراض پوستی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: 6-Formylindolo[3,2-b]Carbazole Accelerates Skin Wound Healing via Activation of ERK, but Not Aryl Hydrocarbon Receptor 6-Formylindolo[3,2-b]Carbazole Accelerates Skin Wound Healing via Activation of ERK, but Not Aryl Hydrocarbon Receptor](/preview/png/8716355.png)
چکیده انگلیسی
Wound healing is an elaborate process composed of overlapping phases, such as proliferation and remodeling, and is delayed in several circumstances, including diabetes. Although several treatment strategies for chronic wounds, such as growth factors, have been applied, further alternatives are required. The skin, especially keratinocytes, is continually exposed to UV rays, which impairs wound healing. 6-Formylindolo[3,2-b]carbazole (FICZ) is a tryptophan photoproduct formed by UV exposure, indicating that FICZ might be one of the effectors of UV radiation. In contrast, treatment with tryptophan, the precursor for FICZ, promoted wound closure in keratinocytes. Therefore, the aim of our study was to determine the role of FICZ in wound healing. Here we showed that FICZ enhanced keratinocyte migration through mitogen-activated protein kinase/extracellular signal-regulated kinase activation, and promoted wound healing in various mouse models, including db/db mice, which exhibit wound healing impairments because of type 2 diabetes. Moreover, FICZ, the endogenous ligand of an aryl hydrocarbon receptor, accelerated migration even in the aryl hydrocarbon receptor knockdown condition and also promoted wound healing in DBA/2 mice, bearing a low-affinity aryl hydrocarbon receptor, suggesting that FICZ enhanced keratinocyte migration in a mitogen-activated protein kinase/extracellular signal-regulated kinase-dependent, but aryl hydrocarbon receptor-independent, manner. The function of FICZ might indicate the possibility of its clinical use for intractable chronic wounds.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Investigative Dermatology - Volume 137, Issue 10, October 2017, Pages 2217-2226
Journal: Journal of Investigative Dermatology - Volume 137, Issue 10, October 2017, Pages 2217-2226
نویسندگان
Saori Morino-Koga, Hiroshi Uchi, Chikage Mitoma, Zhouwei Wu, Mari Kiyomatsu, Yoko Fuyuno, Konosuke Nagae, Mao Yasumatsu, Mary Ann Suico, Hirofumi Kai, Masutaka Furue,