{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:20:32Z","timestamp":1784557232923,"version":"3.55.0"},"reference-count":45,"publisher":"Bioscientifica","issue":"1","license":[{"start":{"date-parts":[[2024,1,1]],"date-time":"2024-01-01T00:00:00Z","timestamp":1704067200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["rem.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,5,7]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>UV irradiation of the skin induces photo damage and generates cytotoxic intracellular reactive oxygen species (ROS), activating the unfolded protein response (UPR) to adapt or reduce these UVB-mediated damages. This study was designed to understand the role of the UPR mediator IRE1\u03b1 in the antioxidant response following UVB irradiation of mouse skin and keratinocytes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We used mice with an epidermal deletion of IRE1\u03b1 and primary mouse keratinocytes to examine effects of UV on different parameters of the antioxidant response in the presence and absence of functional IRE1\u03b1.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In the absence of IRE1\u03b1, PERK activity and protein levels are significantly compromised following UVB irradiation. Additionally, the loss of IRE1\u03b1 suppressed phosphorylation of the PERK target, nuclear factor erythroid-2-related factor 2 (NRF2), and NRF2-dependent antioxidant gene expression after UVB irradiation. Interestingly, IRE1\u03b1-deficient keratinocytes exhibit elevated basal ROS levels, while a robust ROS induction upon UVB exposure is abolished. Because UVB-induced ROS plays an essential role in regulating skin inflammation, we analyzed recruited immune cell populations and the expression of pro-inflammatory cytokines,\n                      <jats:italic>Il-6<\/jats:italic>\n                      and\n                      <jats:italic>Tnf\u03b1<\/jats:italic>\n                      , in mice with epidermally targeted deletion of\n                      <jats:italic>Ire1\u03b1<\/jats:italic>\n                      . Following UVB irradiation, there was significantly less recruitment of neutrophils and leukocytes and reduced expression of pro-inflammatory cytokine genes in the skin of mice lacking IRE1\u03b1. Furthermore, keratinocyte proliferation was also significantly reduced after chronic UVB exposure in the skin of these mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Collectively, our findings indicate that IRE1\u03b1 is essential for basal and UVB-induced oxidative stress response, UV-induced skin immune responses, and keratinocyte proliferation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance statement<\/jats:title>\n                    <jats:p>These findings shed new light on the protective function of IRE1\u03b1 in the response to UV. IRE1\u03b1 plays an important role in the regulation of ROS, PERK stability, and antioxidant gene expression in response to UVB in mouse keratinocytes and epidermis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1530\/rem-23-0030","type":"journal-article","created":{"date-parts":[[2024,5,7]],"date-time":"2024-05-07T07:12:11Z","timestamp":1715065931000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-18","source":"Crossref","is-referenced-by-count":6,"title":["IRE1\u03b1 regulates ROS and immune responses after UVB irradiation"],"prefix":"10.1530","volume":"2024","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1069-0001","authenticated-orcid":true,"given":"Jeongin","family":"Son","sequence":"first","affiliation":[{"name":"The Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park PA, USA"},{"name":"Department of Discovery Protein Science, Amgen Inc., South San Francisco, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jacob T","family":"Bailey","sequence":"additional","affiliation":[{"name":"The Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park PA, USA"},{"name":"Department of Immunology and Microbial Disease, Albany Medical College, Albany, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Worrell","sequence":"additional","affiliation":[{"name":"The Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park PA, USA"},{"name":"University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2675-9301","authenticated-orcid":true,"given":"Adam B","family":"Glick","sequence":"additional","affiliation":[{"name":"The Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"bib1","series-title":"Biochimica et Biophysica Acta. 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