title: Phytosphingosine-1-phosphate represses the hydrogen peroxide-induced activation of c-Jun N-terminal kinase in human dermal fibroblasts through the phosphatidylinositol 3-kinase/Akt pathway.
abstract: Dermal fibroblasts are differentiated mesenchymal cells that regulate the extracellular matrix through the production of dermis components. Dermal fibroblasts can be damaged by reactive oxygen species induced by ultraviolet rays and chemicals. In addition to its effects on the dermis, oxidative stress poses a major threat to organisms and is believed to play an essential role in many disease processes. In this study, we show that human dermal fibroblasts (HDFs) express sphingosine-1-phosphate (S1P) receptors S1P(1), S1P(2), and S1P(3). In addition, cell viability of HDFs is increased by phytosphingosine-1-phosphate (PhS1P) via regulation of the Jun N-terminal kinase (JNK)/Akt pathway. Interestingly, regulation of the JNK/Akt pathway by PhS1P attenuated H(2)O(2)-induced cell growth arrest. Together, our data indicate that PhS1P attenuates H(2)O(2)-induced growth arrest through regulation of the signal molecules Akt and JNK, and suggest that PhS1P may have value as an anti-aging material in cosmetics and medicine.
authors.affiliation: Coreana Cosmetics Co., Ltd., Seonggeo-eup, Seobuk-gu, Cheonan-si, Chungcheongnam-do, Republic of Korea.
authors.forename: Jeong Pyo
authors.initials: JP
authors.lastname: Lee
authors.forename: Hwa Jun
authors.initials: HJ
authors.lastname: Cha
authors.forename: Kwang Sik
authors.initials: KS
authors.lastname: Lee
authors.forename: Kun Kook
authors.initials: KK
authors.lastname: Lee
authors.forename: Ju Hyun
authors.initials: JH
authors.lastname: Son
authors.forename: Kwang Nyeon
authors.initials: KN
authors.lastname: Kim
authors.forename: Dong Kyu
authors.initials: DK
authors.lastname: Lee
authors.forename: Sungkwan
authors.initials: S
authors.lastname: An
mesh_terms: D019588:Aging, Premature / Q000188:drug therapy* / Q000378:metabolism; D048708:Cell Growth Processes / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D020405:Dermis / Q000473:pathology; D004789:Enzyme Activation / Q000187:drug effects; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D006861:Hydrogen Peroxide / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D049349:Receptors, Lysosphingolipid / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D013110:Sphingosine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000081025:Sphingosine-1-Phosphate Receptors
chemical_list: D049349:Receptors, Lysosphingolipid; C477522:S1PR2 protein, human; D000081025:Sphingosine-1-Phosphate Receptors; C117422:phytosphingosine-1-phosphate; D006861:Hydrogen Peroxide; D058539:Phosphatidylinositol 3-Kinase; D051057:Proto-Oncogene Proteins c-akt; D048031:JNK Mitogen-Activated Protein Kinases; D013110:Sphingosine