Compounds > d-ribo-phytosphingosine-1-phosphate

d-ribo-phytosphingosine-1-phosphate and Aging--Premature

d-ribo-phytosphingosine-1-phosphate has been researched along with Aging--Premature* in 1 studies

Other Studies

1 other study(ies) available for d-ribo-phytosphingosine-1-phosphate and Aging--Premature

Article	Year
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. Archives of dermatological research, 2012, Volume: 304, Issue:8 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. Topics: Aging, Premature; Cell Growth Processes; Cell Survival; Cells, Cultured; Dermis; Enzyme Activation; Fibroblasts; Humans; Hydrogen Peroxide; JNK Mitogen-Activated Protein Kinases; Oxidative Stress; Phosphatidylinositol 3-Kinase; Proto-Oncogene Proteins c-akt; Receptors, Lysosphingolipid; Signal Transduction; Sphingosine; Sphingosine-1-Phosphate Receptors	2012

Article

Year

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.

Archives of dermatological research, 2012, Volume: 304, Issue:8

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.

Topics: Aging, Premature; Cell Growth Processes; Cell Survival; Cells, Cultured; Dermis; Enzyme Activation; Fibroblasts; Humans; Hydrogen Peroxide; JNK Mitogen-Activated Protein Kinases; Oxidative Stress; Phosphatidylinositol 3-Kinase; Proto-Oncogene Proteins c-akt; Receptors, Lysosphingolipid; Signal Transduction; Sphingosine; Sphingosine-1-Phosphate Receptors

2012