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Previous studies demonstrate that EGFR in keratinocytes can be activated by UVB and contributes to inflammation. Poly (ADP\u2010ribose) polymerase\u20101 (PARP\u20101) is a nuclear enzyme and plays an essential role in DNA repair under moderate stress. In this study, we set out to understand how PARP\u20101 regulates UVB irradiation\u2010induced skin injury and interplays with EGFR to mediate the inflammation response. We found that PARP\u20101 deficiency exacerbated the UVB\u2010induced inflammation, water loss, and back skin damage in mice. In human primary keratinocytes, UVB can activate PARP\u20101 and enhance DNA damage upon PARP\u20101 gene silencing. Moreover, PARP\u20101 silencing and PARP inhibitor olaparib can suppress UVB\u2010induced COX\u20102 and MMP\u20101 expression, but enhance TNF\u2010\u03b1 and IL\u20108 expression. In addition, EGFR silencing or EGFR inhibition by gefitinib can decrease UVB\u2010induced COX\u20102, TNF\u2010\u03b1, and IL\u20108 expression, suggesting EGFR activation via paracrine action can mediate UVB\u2010induced inflammation responses. Immunoblotting data revealed that PARP\u20101 inhibition decreases UVB\u2010induced EGFR and p38 activation. Pharmacological inhibition of p38 also dramatically led to the attenuation of UVB\u2010induced inflammatory gene expression. Of note, genetic ablation of PARP\u20101 or EGFR can attenuate UVB\u2010induced ROS production, and antioxidant NAC can attenuate UVB\u2010induced EGFR\u2010p38 signaling axis and PARP\u20101 activation. These data suggest the regulatory loops among EGFR, PARP\u20101, and ROS upon UVB stress. PARP\u20101 not only serves DNA repair function but also orchestrates interactions to EGFR transactivation and ROS production, leading to p38 signaling for inflammatory gene expression in keratinocytes.<\/jats:p>","DOI":"10.1096\/fj.202002285rr","type":"journal-article","created":{"date-parts":[[2021,2,13]],"date-time":"2021-02-13T22:39:57Z","timestamp":1613255997000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["PARP\u20101 involves in UVB\u2010induced inflammatory response in keratinocytes and skin injury via regulation of ROS\u2010dependent EGFR transactivation and p38 signaling"],"prefix":"10.1096","volume":"35","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8566-7696","authenticated-orcid":false,"given":"Ling\u2010Ya","family":"Chiu","sequence":"first","affiliation":[{"name":"Department of Pharmacology, College of Medicine National Taiwan University Taipei Taiwan"},{"name":"Department of Medical 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