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Immunohistochemistry and Western analysis indicated that COX\u20102, and not COX\u20101, was induced by UVB (2.5 or 5.0 kJ\/m<jats:sup>2<\/jats:sup>), but that COX\u20101 remained the major source of prostaglandin E<jats:sub>2<\/jats:sub> production. UVB exposure significantly increased epidermal apoptosis in all genotypes compared to untreated mice. However, while the number of apoptotic cells in WT and COX\u20101\u2212\/\u2212 mice were about equal, the number of apoptotic cells was 2.5\u2010fold greater in COX\u20102\u2212\/\u2212 mice. Apoptosis in WT and COX\u20102\u2212\/\u2212 mice peaked at 24 h post\u2010exposure. The increased apoptosis and reduced proliferation in COX\u20102\u2212\/\u2212 mice resulted in about a 50% decrease in epidermal thickness at 24\u201348 h post\u2010exposure compared to about a 50% increase in epidermal thickness in WT mice. UVB\u2010induced cell replication, as measured by BrdU labeling, was reduced in COX\u20102\u2212\/\u2212 compared to WT mice at 24\u201396 h. However, by 96 h post\u2010exposure, both WT and COX\u20102\u2212\/\u2212 mice showed epidermal hyperplasia. The data indicate that COX\u20102 induction initially protects against the acute sunburn effects of UVB, but that continuous induction of COX\u20102 may contribute to skin cancer in chronic UVB exposure. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/mc.20290","type":"journal-article","created":{"date-parts":[[2007,1,19]],"date-time":"2007-01-19T18:19:09Z","timestamp":1169230749000},"page":"354-362","source":"Crossref","is-referenced-by-count":27,"title":["Cyclooxygenase\u20102 deficiency increases epidermal apoptosis and impairs recovery following acute UVB exposure"],"prefix":"10.1002","volume":"46","author":[{"given":"Jacqueline K.","family":"Akunda","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kyung\u2010Soo","family":"Chun","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alisha 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