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Prakash Radhakrishnan Sally Dabelsteen Frey Brus Madsen Chiara Francavilla Katharina L. Kopp Catharina Steentoft Sergey Y. Vakhrushev Jesper V. Olsen Lars Hansen Eric P. Bennett Anders Woetmann Guangliang Yin Longyun Chen Haiyan Song Mads Bak Ryan A. Hlady Staci L. Peters Rene Opavsky Christenze Thode Klaus Qvortrup Katrine T.-B. G. Schjoldager Henrik Clausen Michael A. Hollingsworth Hans H. Wandall 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(39):E4066-E4075
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Q. Liu H. Wang X. Wang M. Lu X. Tan L. Peng F. Tan T. Xiao S. Xiao Y. Xia 《Clinical and experimental immunology》2020,199(1):56-67
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) acts through its receptor fibroblast growth factor inducible 14 (Fn14), and participates in skin inflammation. Both TWEAK and Fn14 are highly expressed in skin lesions of patients with atopic dermatitis. The purpose of this study was to further explore the effect of Fn14 inhibition on experimental atopic dermatitis. Experimental atopic dermatitis was induced in the wild-type and Fn14 knock-out BALB/c mice. The effect of TWEAK/Fn14 interaction on keratinocytes was studied in an in-vitro model of atopic dermatitis. Fn14 deficiency ameliorates skin lesions in the mice model, accompanied by less infiltration of inflammatory cells and lower local levels of proinflammatory cytokines, including TWEAK, TNF-α and interleukin (IL)-17. Fn14 deficiency also attenuates the up-regulation of TNFR1 in skin lesions of atopic dermatitis. Moreover, topical TWEAK exacerbates skin lesion in the wild-type but not in the Fn14 knock-out mice. In vitro, TWEAK enhances the expressions of IL-17, IL-18 and IFN-γ in keratinocytes under atopic dermatitis-like inflammation. These results suggest that Fn14 deficiency protects mice from experimental atopic dermatitis, involving the attenuation of inflammatory responses and keratinocyte apoptosis. In the context of atopic dermatitis-like inflammation, TWEAK modulates keratinocytes via a TNFR1-mediated pathway. 相似文献
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Objective:The plant polyphenol resveratrol(3,4',5-trihydroxystilbene)(RSV)has been proposed for use because of its protective effect on ultraviolet(UV)-induced ... 相似文献
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Mee Sook Jun Mi Hee Kwack Moon Kyu Kim Jung Chul Kim Young Kwan Sung 《ANNALS OF DERMATOLOGY》2020,32(5):388
BackgroundParticulate matters (PM) comprise a heterogeneous mixture of particles suspended in air. A recent study found that urban PMs may penetrate into hair follicles via transfollicular and transdermal routes in dorsal skin.ObjectiveTo investigate the effects of PM on ex vivo cultured human scalp hair follicles and hair follicular keratinocytes in vitro.MethodsTUNEL staining was employed to check cells undergoing apoptosis in cultured hair follicles after PM treatment. MTT assay was employed to check cell viability after PM treatment. Quantitative real-time PCR analysis was employed to quantitate the expression of inflammatory genes, matrix metalloproteinases (MMPs), and Duox1. Inflammatory cytokine levels were measured by ELISA after PM treatment. The level of reactive oxygen species (ROS) production was measured using a chemical fluorescent probe by a fluorescence plate reader.ResultsAbundant TUNEL-positive cells were observed in the keratinocyte region of hair including the epidermis, sebaceous gland, outer root sheath (ORS), inner root sheath (IRS), and bulb region. The viability of follicular cells, including the ORS, was found to be decreased upon PM exposure. mRNA expression and protein levels of inflammatory response genes and MMPs were upregulated in a dose-dependent manner by PM treatment. ROS levels were also increased by PM.ConclusionThese data strongly suggest that penetrated PMs from air pollution may cause apoptotic cell death to follicular keratinocytes by increased production of ROS and inflammatory cytokines, which could impair hair growth. 相似文献
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