PMID- 18337615 OWN - NLM STAT- MEDLINE DCOM- 20080805 LR - 20220311 IS - 0022-2275 (Print) IS - 0022-2275 (Linking) VI - 49 IP - 6 DP - 2008 Jun TI - Phosphatidylserine prevents UV-induced decrease of type I procollagen and increase of MMP-1 in dermal fibroblasts and human skin in vivo. PG - 1235-45 LID - 10.1194/jlr.M700581-JLR200 [doi] AB - In an effort to find topical agents that prevent or retard cutaneous aging, seven functional lipids were screened for their procollagen-upregulating and matrix metalloproteinase (MMP)-1-downregulating activities in human dermal fibroblasts by Western blotting. The preventive effect on ultraviolet (UV)-induced decrease of procollagen was demonstrated in phosphatidylserine (PS), lysophosphatidylserine (LPS), lysophosphatidic acid (LPA), N-acetyl phytosphingosine (NAPS), and tetraacetyl phytosphingosine (TAPS). Furthermore, PS, LPS, and LPA upregulated procollagen expression in unirradiated basal conditions. The inhibitory effect on UV-induced MMP-1 expression was seen in NAPS, TAPS, LPA, PS, lysophosphatidylglycerol, and LPS. PS was chosen as the most suitable candidate anti-aging chemical for the subsequent in vivo studies. We investigated the effects of PS on acute UV response and chronologic skin aging by topically applying it to young skin before UV irradiation and to aged human skin, respectively. Real-time PCR and Western blot revealed that in the young skin, PS treatment prevented UV-induced reduction in procollagen expression and inhibited UV-induced MMP-1 expression. PS also blocked UV-induced IL-6 and COX-2 gene expression in cultured fibroblasts dose-dependently. In the aged skin, PS caused increased procollagen transcription and procollagen immunostaining in the upper dermis, and a significant decrease in MMP-1 expression at both mRNA and protein levels. These results indicate that topical PS has anti-skin-aging properties and point to the potential use of PS as a therapeutic agent in the prevention and treatment of cutaneous aging. FAU - Cho, Soyun AU - Cho S AD - Department of Dermatology, Seoul National University College of Medicine, Seoul, Korea. FAU - Kim, Hyeon Ho AU - Kim HH FAU - Lee, Min Jung AU - Lee MJ FAU - Lee, Serah AU - Lee S FAU - Park, Chang-Seo AU - Park CS FAU - Nam, Sang-June AU - Nam SJ FAU - Han, Jeong-Jun AU - Han JJ FAU - Kim, Jin-Wook AU - Kim JW FAU - Chung, Jin Ho AU - Chung JH LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20080312 PL - United States TA - J Lipid Res JT - Journal of lipid research JID - 0376606 RN - 0 (Collagen Type I) RN - 0 (DNA Primers) RN - 0 (Interleukin-1alpha) RN - 0 (Interleukin-6) RN - 0 (Phosphatidylserines) RN - 0 (RNA, Messenger) RN - 0 (Tumor Necrosis Factor-alpha) RN - EC 1.14.99.1 (Cyclooxygenase 2) RN - EC 3.4.24.7 (Matrix Metalloproteinase 1) SB - IM MH - Base Sequence MH - Blotting, Western MH - Cells, Cultured MH - Collagen Type I/genetics/*metabolism MH - Cyclooxygenase 2/genetics MH - DNA Primers MH - Fibroblasts/enzymology/metabolism MH - Humans MH - Immunohistochemistry MH - Interleukin-1alpha/metabolism MH - Interleukin-6/genetics MH - Matrix Metalloproteinase 1/genetics/*metabolism MH - Phosphatidylserines/*pharmacology MH - Polymerase Chain Reaction MH - RNA, Messenger/genetics MH - Skin/cytology/enzymology/*metabolism MH - Tumor Necrosis Factor-alpha/metabolism MH - *Ultraviolet Rays EDAT- 2008/03/14 09:00 MHDA- 2008/08/06 09:00 CRDT- 2008/03/14 09:00 PHST- 2008/03/14 09:00 [pubmed] PHST- 2008/08/06 09:00 [medline] PHST- 2008/03/14 09:00 [entrez] AID - S0022-2275(20)42368-5 [pii] AID - 10.1194/jlr.M700581-JLR200 [doi] PST - ppublish SO - J Lipid Res. 2008 Jun;49(6):1235-45. doi: 10.1194/jlr.M700581-JLR200. Epub 2008 Mar 12.