811 UVB initiates skin inflammation by promoting keratinocyte ferroptosis
نویسندگان
چکیده
Epidermis, composed primarily of the keratinocytes, is subjected to ultraviolet radiation (UVR)-induced oxidative and genotoxic stresses. That keratinocytes are initial source pro-inflammatory mediators in skin after UVR exposure has been well established. Ultraviolet B (UVB) a strong initiator cutaneous inflammation, contributes etiology exacerbation several diseases, such as lupus erythematosus. However, mechanism UVB-induced inflammation remains unclear. Utilizing primary human epidermal explants, we found that ferroptosis, type non-apoptotic programmed cell death associated with an excessive phospholipid peroxidation, activated UVB exposure. We further keratinocyte susceptibility ferroptosis dictated by extent lipid peroxidation dysregulation glutathione system. Ferroptosis inhibition prevented HMGB1 release from protected UVB-irradiated inflammation. While apoptosis pyroptosis were also detectable exposure, determined plays dominant role initiating Our findings have significant implications for prevention treatment wide range diseases fostered
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ژورنال
عنوان ژورنال: Journal of Investigative Dermatology
سال: 2022
ISSN: ['1523-1747', '0022-202X']
DOI: https://doi.org/10.1016/j.jid.2022.05.825