Adipose-derived stem cell conditioned medium accelerates keratinocyte differentiation via the upregulation of miR-24 Gimoon Seo, Eunhye Oh, Mihee Yun, Ji-Young Lee, Joon Sung Bae, Kwon Joo, Gue Tae Chae and Seong-Beom Lee Institute of Hansen’s Disease, College of Medicine, The Catholic University of Korea, Seoul, Korea; Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul, Korea; JK Plastic Surgery Center, Gangnam-gu, Seoul, Korea Correspondence: Seong-Beom Lee, Institute of Hansen’s Disease, Department of Pathology, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 137-701, Korea, Tel.: +82-2-2258-7313, Fax: +82-2-595-2241, e-mail: sblee@catholic.ac.kr

It has been suggested that free fatty acids (FFA) such as palmitate, which are secreted from enlarged adipocytes in the subcutaneous fat of obese subjects, serve as a link between obesity and altered skin functions. Cyclooxygenease-2 (COX-2) and prostanoids participate in the induction of impaired dermal function. In the current study, we investigated the issue of whether palmitate induces COX-2 expression via the sphingolipid pathway-mediated activation of NF-κB or mitogen-activated protein kinase (MAPK) pathways in human dermal fibroblasts. Palmitate treatment significantly induced COX-2 expression and prostaglandin E2 (PGE2) release in human dermal fibroblasts. In addition, pre-treatment with triacsin C, an inhibitor of acyl-CoA synthetase in de novo ceramide synthesis, was found to reduce palmitate-induced COX-2 expression and PGE2 release in human dermal fibroblast. The findings also show that palmitate-induced COX-2 expression and PGE2 release are mediated by the NF-κB, p38, and extracellular signal-regulated kinase (ERK) MAPK pathways. These findings point to a new mechanism for explaining the link between increased FFAs in obesity and impaired dermal function.