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We previously demonstrated that histone deacetylase inhibitors (HDACi) induce the mRNA and protein expression of AQP3, in part through the p53 family, transcription factors for which acetylation is known to affect their regulatory activity. Another set of transcription factors previously shown to induce AQP3 expression and\/or regulate skin function are the peroxisome proliferator\u2010activated receptors (PPARs). Since there are reports that PPARs are also acetylated, we examined the involvement of these nuclear hormone receptors in HDACi\u2010induced AQP3 expression. We first verified that a PPAR\u03b3 agonist upregulated AQP3 mRNA and protein levels and that this increase was blocked by a PPAR\u03b3 antagonist. We then showed that the PPAR\u03b3 antagonist also inhibited AQP3 expression induced both by a broad\u2010spectrum HDACi and an HDAC3\u2010selective inhibitor. Interestingly, a PPAR\u03b1 antagonist also inhibited HDACi\u2010induced AQP3 expression. These antagonist effects were observed in both primary mouse and normal human keratinocytes. Furthermore, PPAR\u03b3 overexpression enhanced HDACi\u2010stimulated AQP3 mRNA levels. Thus, our results suggest that PPAR\u03b3 and\/or PPAR\u03b1 may play a role in regulating AQP3 levels in the skin; based on the ability of PPAR agonists to promote epidermal differentiation and\/or inhibit proliferation, topical PPAR agonists might be considered as a therapy for hyperproliferative skin disorders, such as psoriasis.<\/jats:p>","DOI":"10.1111\/exd.14080","type":"journal-article","created":{"date-parts":[[2020,1,31]],"date-time":"2020-01-31T04:08:25Z","timestamp":1580443705000},"page":"380-386","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Keratinocyte aquaporin\u20103 expression induced by histone deacetylase inhibitors is mediated in part by peroxisome proliferator\u2010activated receptors (PPARs)"],"prefix":"10.1111","volume":"29","author":[{"given":"Rong","family":"Yang","sequence":"first","affiliation":[{"name":"Department of Physiology Jianghan University Medical School Wuhan China"},{"name":"Department of Physiology Medical College of Georgia at Augusta University Augusta GA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shinjini","family":"Chowdhury","sequence":"additional","affiliation":[{"name":"Department of Physiology Medical College of Georgia at Augusta University Augusta GA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3664-5025","authenticated-orcid":false,"given":"Vivek","family":"Choudhary","sequence":"additional","affiliation":[{"name":"Department of Physiology Medical College of Georgia at Augusta University Augusta GA USA"},{"name":"Charlie Norwood VA Medical Center Augusta GA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xunsheng","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Physiology Medical College of Georgia at Augusta University Augusta GA USA"},{"name":"Charlie Norwood VA Medical Center Augusta GA 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