[논문]Sphigosine-1-Phosphate-Induced ERK Activation Protects Human Melanocytes from UVB-Induced Apoptosis

Kim, Dong-Seok; Kim, Sook-Young; Lee, Jai-Eun; Kwon, Sun-Bang; Joo, Young-Hyun; Youn, Sang-Woong; Park, Kyoung-Chan

doi:10.1007/bf02976685

Sphigosine-1-Phosphate-Induced ERK Activation Protects Human Melanocytes from UVB-Induced Apoptosis 원문보기

Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea, v.26 no.9, 2003년, pp.739 - 746

Kim, Dong-Seok (Research Division for Human Life Sciences, Seoul National University, Department of Dermatology, Seoul National University College of Medicine) , Kim, Sook-Young (Department of Dermatology, Seoul National University College of Medicine) , Lee, Jai-Eun (Department of Dermatology, Seoul National University College of Medicine) , Kwon, Sun-Bang (Department of Dermatology, Seoul National University College of Medicine) , Joo, Young-Hyun (Department of Dermatology, Seoul National University College of Medicine) , Youn, Sang-Woong (Department of Dermatology, Seoul National University College of Medicine) , Park, Kyoung-Chan (Department of Dermatology, Seoul National University College of Medicine)

Abstract ▼ AI-Helper

Ultraviolet B (UVB) is known to induce apoptosis in human melanocytes. Here we show the cytoprotective effect of sphingosine-1-phosphate (S1P) against UVB-induced apoptosis. We also show that UVB-induced apoptosis of melanocytes is mediated by caspase-3 activation and poly(ADP-ribose) polymerase (PARP) cleavage, and that S1P prevents apoptosis by inhibiting this apoptotic pathway. We further investigated three major mitogen-activated protein (MAP) kinases after UVB irradiation. UVB gradually activated c-Jun N-terminal kinase (JNK) and p38 MAP kinase, while extracellular signal-regulated protein kinase (ERK) was inactivated transiently. Blocking of the p38 MAP kinase pathway using SB203580 promoted cell survival and inhibited the activation of caspase-3 and PARP cleavage. These results suggest that p38 MAP kinase activation may play an important role in the UVB-induced apoptosis of human melanocytes. To explain this cytoprotective effect, we next examined whether S1P could inhibit UVB-induced JNK and p38 MAP kinase activation. However, S1P was not found to have any influence on UVB-induced JNK or p38 MAP kinase activation. In contrast, S1P clearly stimulated the phosphorylation of ERK, and the specific inhibition of the ERK pathway using PD98059 abolished the cytoprotective effect of S1P. Based on these results, we conclude that the activation of p38 MAP kinase plays an important role in UVB-induced apoptosis, and that S1P may show its cytoprotective effect through ERK activation in human melanocytes.

주제어

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가설 설정

In this study, we investigated the UV-induced apoptosis of melanocytes and found that S1P can protect human melanocytes against apoptotic cell death. In order to understand the signaling mechanism of melanocyte apoptosis, changes of signaling kinases were inve옹tigated after UVB irradiation and S1P treatment.

대상 데이터

Cells were maintained in a humidified incubator in 5% CO₂ at 37℃. Second and third passage melanocytes were used in the experiments.

데이터처리

Differences between results were assessed for significance using the ShJde가s f-test.

이론/모형

Cell viability was determined using a crystal violet assay(Dooley et al., 1994). After incubating with the test substances for 24 h, the culture medium was removed.

성능/효과

important for UVB-induced apoptosis. In conclusion, we have demonstrated that S1P protects h니man melanocytes frorr UVB-induced apoptosis 그nd that it exerts its cytoprotective effects mainly via ERK activation.
, 2002). Our results d이monstrate that UVB irradiation resulted in the activation of JNK and p38 MAP kinase and a transient inactivation of ERK, whereas S1P potently stimulated the phosphorylation of ERK. JNK and p38 MAP kinase are important mediators of stress signals that ultimately lead to apoptosis (Harper and LoGrasso, 2001; Peus et al.
activation and p38 MAP kinase inhibition. Our results showed that the combination of SB203580 and S1P increased cell survival slightly. Th니s, JNK involvement could explain the partial cytoprotective effect of S1P and SB203580.
, 1996). Our results, obtained using human melanocytes show that UVB irradiation leads to the sustained activation of JNK and p38 MAP kinase, while ERK is transiently inactivated. Moreover, whereas S1P did not suppress the activation of JNK or p38 MAP kinase, it induced the activation of ERK.

후속연구

These results indicate that p38 MAP kinase is important in the UVB-mediated apoptosis of melanocytes. However, the role of JNK needs further investigation.

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