A polypeptide from Chlamys farreri inhibits UVB-induced HaCaT cells apoptosis via the Apaf-1/caspase-9 and Smac/XIAP signaling pathway

详细信息    查看全文

• 作者：Xiaojin Liu (1)
  Wencheng Wang (2)
  Hongjiang Wang (1)
  Lanlan Zhang (1)
  Leqian Liu (3)
  Yuejun Wang (4)
  Chunbo Wang (1)
  
• 关键词：polypeptide from Chlamys farreri (PCF) ; UVB ; apoptosis ; Smac/XIAP ; Apaf ; 1/caspase ; 9
• 刊名：Chinese Journal of Oceanology and Limnology
• 出版年：2009
• 出版时间：September 2009
• 年：2009
• 卷：27
• 期：3
• 页码：587-593
• 全文大小：567KB
• 参考文献：1. Adrain C, Martin S J. 2001. The mitochondrial apoptosome: A killer unleashed by the cytochrome seas. / Trends Biochem Sci., 26: 390-97. CrossRef
  2. Bratton S B, Cohen G M. 2001. Apoptotic death sensor: an organelle’s alter ego / Trends Pharmacol Sci., 22: 306-15. CrossRef
  3. Chai J, Du C, Wu J W, Kyin S, Wang X, Shi Y. 2000. Structural and biochemical basis of apoptotic activation by Smac / DIABLO. / Nature, 406: 855-62. CrossRef
  4. Deveraux Q L, Reed J C. 1999. IAP family proteins-suppressors of apoptosis. / Genes Dev, 13: 239-52. CrossRef
  5. Deveraux Q L, Roy N, Stennicke H R, Van Arsdale T, Zhou Q, Srinivasula S M, Alnemri E S, Salvesen G S, Reed J C. 1998. IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases. / J. Embo., 17: 2 215- 223. CrossRef
  6. Du C, Fang M, Li Y, Li L, Wang X. 2000. Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition. / Cell, 102: 33-2. CrossRef
  7. Ekert P G, Silke J, Hawkins C J, Verhagen A M, Vaux D L. 2001. / J. Cell Biol., 152, 483-90. CrossRef
  8. Kim H E, Jiang X, Du F, Wang X. 2008. PHAPI, CAS, and Hsp 70 promote apoptosome formation by preventing Apaf-1 aggregation and enhancing nucleotide exchange on Apaf-1. / Mol. Cell., 30(2): 239-7. CrossRef
  9. Li B H, Zhou Y B, Guo S B, Wang C B. 2007. Polypeptide from / Chlamys farreri inhibits UVB-induced HaCaT cells apoptosis via inhibition CD95 pathway and reactive oxygen species. / Free Radic Res., 41(11): 1 224- 232. CrossRef
  10. Li P, Nijhawan D, Budihardjo I, Srinivasula S M, Ahmad M, Alnemri E S, Wang X. 1997. Cytochrome c and dATP dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. / Cell, 91: 479-89.
  11. Murphy G, Young A R, Wulf H C, Kulms D, Schwarz T. 2001. The molecular determinants of sunburn cell formation. / Exp. Dermatol. 10: 155-60. CrossRef
  12. Nilkantha Sen, Benu Brata Das, Agneyo Ganguly, Tanmoy Mukherjee, Santu Bandyopadhyay, Hemanta K. Majumder. 2004. Camptothecin-induced Imbalance inIntracellular Cation Homeostasis Regulates Programmed Cell Death in Unicellular Hemoflagellate Leishmania donovani. / J. Biol. Chem., 279(50): 523 66-2 375. CrossRef
  13. Riedl S J, Salvesen G S. 2007. The apoptosome: signaling platform for cell death, / Nat. Rev. Mol. Cell Biol, 8: 405-13. CrossRef
  14. Shimizu S, Narita M, Tsujimoto Y. 1999. Bcl-1 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC. / Nature, 399: 483-87. CrossRef
  15. Sitailo L A, Tibudan S S, Denning M F. 2002. Activation of caspase-9 is required for UV-induced apoptosis of human keratinocytes. / J. Biol. Chem. 277: 19 346-9 352. CrossRef
  16. Soengas M S, Alarcon R M, Yoshida H, Giaccia A J, Hakem R, Mak T W, Lowe S W. 1999. Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition. / Science, 284(5411): 156-59. CrossRef
  17. Steller H. 1995. Mechanisms and genes of cellular suicide. / Science, 267: 1 445- 449. CrossRef
  18. Suzuki Y, Takahashi-Niki K, Akagi T, Hashikawa T, Takahashi R. 2004. Mitochondrial protease Omi/HtrA2 enhances caspase activation through multiple pathways. / Cell Death and Differentiation, 11: 208-16. CrossRef
  19. Takasawa R, Nakamura H, Mori T, Tanuma S. 2005. Differential apoptotic pathways in human keratinocyte HaCaT cells exposed to UVB and UVC. / Apoptosis, 10: 1 121- 130. CrossRef
  20. Takasawa R, Tanuma S. 2003. Sustained release of Smac/DIABLO from mitochondria commits to undergo UVB-induced apoptosis. / Apoptosis, 8: 291-99. CrossRef
  21. Wang C B, Huang M Q, Tao G L, Yu G Y, Han Z W, Yang Z H, Wang Y J. 2004. Polypeptide from / Chlamys farreri protects HaCaT cells from UVB-induced apoptosis. / Chemico-Biological Interactions, 147: 119-27. CrossRef
  22. Wang X Q, Xiao A Y. Christian S, Krzystztof H, Yang A Z, Goldberg M P., Choi D W, Yu S P. 2003. Apoptotic insults impair Na⁺, K⁺-ATPase activity as a mechanism of neuronal death mediated by concurrent ATP deficiency and oxidant stress. / J. Cell Science, 116: 2 099- 110
  
• 作者单位：Xiaojin Liu (1)
  Wencheng Wang (2)
  Hongjiang Wang (1)
  Lanlan Zhang (1)
  Leqian Liu (3)
  Yuejun Wang (4)
  Chunbo Wang (1)
  
  1. Department of Pharmacology, Medical College of Qingdao University, Qingdao, 266071, China
  2. Medical College, Taishan University, Taian, 271000, China
  3. Department of Biological Sciences, East Tennessee State University, Johnson City, USA
  4. Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Qingdao, 266071, China
  
• ISSN：1993-5005

文摘

A novel marine active polypeptide (PCF), isolated from the gonochoric Chinese scallop, Chlamys farreri, has potential antioxidant and anti-apoptotic activity against ultraviolet irradiation. We investigated whether UVB-induced HaCaT cell apoptosis occurs via the mitochondrial pathways Apaf-1/caspase-9 and Smac/XIAP/caspase-3. We then investigated the molecular mechanisms controlling the anti-apoptotic effect of PCF. Pre-treatment with PCF and caspase-9 inhibitor significantly inhibited UVB-induced apoptosis in HaCaT cells based on a DNA fragmentation assay and Hoechst 33258 staining. The expression of Apaf-1 and the cleavage of procaspase-9 were dose-dependently reduced by 1.42-.96 mmol/L PCF pretreatment in UVB-irradiated HaCaT cells. This was followed by inhibition of cleavage of procaspase-3, whose activation induced cell apoptosis. Meanwhile, PCF significantly and dose-dependently enhanced the activation of ATPase. Furthermore, we demonstrated that PCF strongly inhibited the release of Smac from the mitochondria to cytosol by reducing the degradation of XIAP dose-dependently. We conclude that the protective effect of PCF against UVB irradiation in HaCaT cells may be attributed to the inhibition of the Apaf-1/caspase-9 and Smac/XIAP/caspase-3 apoptotic signaling pathways.