The Roles of the Interaction of BCL2-Antagonist/Killer 1, Apoptotic Peptidase Activating Factor 1 and Selenium in the Pathogenesis of Kashin–Beck Disease

详细信息    查看全文

• 作者：Sen Wang ; Chen Duan ; Feng Zhang ; Xi Wang ; Xiong Guo
• 关键词：Selenium ; Apoptosis signalling pathway ; Chondrocyte ; APAF1 ; BAK1 ; Kashin–Beck disease (KBD)
• 刊名：Biological Trace Element Research
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：170
• 期：1
• 页码：17-24
• 全文大小：1,036 KB
• 参考文献：1.Wang S, Duan C, Zhang F, Ma W, Guo X (2013) Regulatory gene networks and signaling pathways from primary osteoarthritis and Kashin-Beck disease, an endemic osteoarthritis, identified by three analysis software. Gene 1(512):89–96. doi:10.​1016/​j.​gene.​2012.​10.​006 CrossRef
  2.Schepman K, Engelbert RH, Visser MM, Yu C, de Vos R (2011) Kashin Beck disease: more than just osteoarthrosis: a cross-sectional study regarding the influence of body function-structures and activities on level of participation. Int Orthop 5(35):767–776. doi:10.​1007/​s00264-010-1043-3 CrossRef
  3.Yao Y, Pei F, Kang P (2011) Selenium, iodine, and the relation with Kashin-Beck disease. Nutrition 11-12(27):1095–1100. doi:10.​1016/​j.​nut.​2011.​03.​002 CrossRef
  4.Zhao ZJ, Li Q, Yang PZ, Wang H, Kong LC, Wang LH, Sun LY (2013) Selenium: a protective factor for Kaschin-Beck disease in Qing-Tibet Plateau. Biol Trace Elem Res 1-3(153):1–4. doi:10.​1007/​s12011-013-9686-8 CrossRef
  5.Wang J, Li H, Li Y, Yu J, Yang L, Feng F, Chen Z (2013) Speciation, distribution, and bioavailability of soil selenium in the Tibetan plateau Kashin-Beck disease area—a case study in Songpan County, Sichuan Province, China. Biol Trace Elem Res 1-3(156):367–375. doi:10.​1007/​s12011-013-9822-5 CrossRef
  6.Moreno-Reyes R, Mathieu F, Boelaert M, Begaux F, Suetens C, Rivera MT, Neve J, Perlmutter N, Vanderpas J (2003) Selenium and iodine supplementation of rural Tibetan children affected by Kashin-Beck osteoarthropathy. Am J Clin Nutr 1(78):137–144
  7.Meng F, Fu Y , Wang L (2001) The effect evaluation of the prevention of Kashin-Beck disease by the change of food and selenium supplementary. Chin J Ctrl Endem Dis 3 (26):188-190
  8.Wang HY, Chen Z (2008) The paired study on the relationship between KBD and Selenium in hair. Chin J Ctrl Endem Dis 1(23):59–60
  9.Yang J, Wang T, Wu C, Liu C (2010) Selenium level surveillance for the year 2007 of Keshan disease in endemic areas and analysis on surveillance results between 2003 and 2007. Biol Trace Elem Res 1-3(138):53–59. doi:10.​1007/​s12011-010-8609-1 CrossRef
  10.Xiong YM, Mo XY, Zou XZ, Song RX, Sun WY, Lu W, Chen Q, Yu YX, Zang WJ (2010) Association study between polymorphisms in selenoprotein genes and susceptibility to Kashin-Beck disease. Osteoarthr Cartil 6(18):817–824. doi:10.​1016/​j.​joca.​2010.​02.​004 CrossRef
  11.Du XH, Dai XX, Xia SR, Zou XZ, Yan SW, Mo XY, Lu BG, Xiong YM (2012) SNP and mRNA expression for glutathione peroxidase 4 in Kashin-Beck disease. Br J Nutr 2(107):164–169. doi:10.​1017/​S000711451100270​4
  12.Downey CM, Horton CR, Carlson BA, Parsons TE, Hatfield DL, Hallgrimsson B, Jirik FR (2009) Osteo-chondroprogenitor-specific deletion of the selenocysteine tRNA gene, Trsp, leads to chondronecrosis and abnormal skeletal development: a putative model for Kashin-Beck disease. PLoS Genet 8(5):e1000616. doi:10.​1371/​journal.​pgen.​1000616 CrossRef
  13.Moreno-Reyes R, Egrise D, Neve J, Pasteels JL, Schoutens A (2001) Selenium deficiency-induced growth retardation is associated with an impaired bone metabolism and osteopenia. J Bone Miner Res 8(16):1556–1563. doi:10.​1359/​jbmr.​2001.​16.​8.​1556 CrossRef
  14.Wang S, Guo X, Wang W, Wang S (2012) Genome-wide study identifies the regulatory gene networks and signaling pathways from chondrocyte and peripheral blood monocyte of Kashin-Beck disease. Genes Cells 8(17):619–632. doi:10.​1111/​j.​1365-2443.​2012.​01620.​x CrossRef
  15.Liu JT, Guo X, Ma WJ, Zhang YG, Xu P, Yao JF, Bai YD (2010) Mitochondrial function is altered in articular chondrocytes of an endemic osteoarthritis, Kashin-Beck disease. Osteoarthr Cartil 9(18):1218–1226. doi:10.​1016/​j.​joca.​2010.​07.​003 CrossRef
  16.Zheng J, Wu C, Ma W, Zhang Y, Hou T, Xu H, Wu S, Yao X, Guo X (2013) Abnormal expression of chondroitin sulphate N-acetylgalactosaminyltransferase 1 and hapln-1 in cartilage with Kashin-Beck disease and primary osteoarthritis. Int Orthop 10(37):2051–2059. doi:10.​1007/​s00264-013-1937-y CrossRef
  17.Gogada R, Prabhu V, Amadori M, Scott R, Hashmi S, Chandra D (2011) Resveratrol induces p53-independent, X-linked inhibitor of apoptosis protein (XIAP)-mediated Bax protein oligomerization on mitochondria to initiate cytochrome c release and caspase activation. J Biol Chem 33(286):28749–28760. doi:10.​1074/​jbc.​M110.​202440 CrossRef
  18.Underbrink MP, Howie HL, Bedard KM, Koop JI, Galloway DA (2008) E6 proteins from multiple human betapapillomavirus types degrade Bak and protect keratinocytes from apoptosis after UVB irradiation. J Virol 21(82):10408–10417. doi:10.​1128/​JVI.​00902-08 CrossRef
  19.Chen M, Huang L, Shabier Z, Wang J (2007) Regulation of the lifespan in dendritic cell subsets. Mol Immunol 10(44):2558–2565. doi:10.​1016/​j.​molimm.​2006.​12.​020 CrossRef
  20.Radetzki S, Kohne CH, von Haefen C, Gillissen B, Sturm I, Dorken B, Daniel PT (2002) The apoptosis promoting Bcl-2 homologues Bak and Nbk/Bik overcome drug resistance in Mdr-1-negative and Mdr-1-overexpressing breast cancer cell lines. Oncogene 2(21):227–238. doi:10.​1038/​sj.​onc.​1205010 CrossRef
  21.Kuwano K, Yoshimi M, Maeyama T, Hamada N, Yamada M, Nakanishi Y (2005) Apoptosis signaling pathways in lung diseases. Med Chem 1(1):49–56CrossRef PubMed
  22.Herr I, Debatin KM (2001) Cellular stress response and apoptosis in cancer therapy. Blood 9(98):2603–2614CrossRef
  23.Kumamoto H, Ooya K (2005) Detection of mitochondria-mediated apoptosis signaling molecules in ameloblastomas. J Oral Pathol Med 9(34):565–572. doi:10.​1111/​j.​1600-0714.​2005.​00354.​x CrossRef
  24.Pasteels JL, Liu FD, Hinsenkamp M, Rooze M, Mathieu F, Perlmutter N (2001) Histology of Kashin-Beck lesions. Int Orthop 3(25):151–153CrossRef
  
• 作者单位：Sen Wang (1)
  Chen Duan (1)
  Feng Zhang (1)
  Xi Wang (1)
  Xiong Guo (1)
  
  1. School of Public Health, Health Science Center of Xi’an Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, No. 76 Yanta West Road, Xi’an, Shaanxi, 710061, People’s Republic of China
  
• 刊物主题：Biochemistry, general; Biotechnology; Nutrition; Oncology;
• 出版者：Springer US
• ISSN：1559-0720

文摘

BCL2-antagonist/killer 1 (BAK1) and apoptotic peptidase activating factor 1 (APAF1) are significant genes in apoptosis signalling pathway of Kashin–Beck disease (KBD). We aimed to verify the protein expression levels of BAK1 and APAF1 in the cartilage and chondrocytes of patients with KBD. Additionally, we explored the relationship between the levels of these proteins and selenium concentration. Chondrocytes was cultured and treated with sodium selenite in vitro. Immunohistochemistry and Western blotting were used to verify the expression levels of BAK1 and APAF1. Compared with the control samples, APAF1 was upregulated and BAK1 was downregulated in the cartilage and chondrocytes of KBD patients. APAF1 expression was higher in the middle and deep zone in the KBD cartilage. APAF1 levels decreased gradually with the increasing selenium concentration (0.05, 0.10 and 0.25 mg/L). BAK1 expression in the 0.25 mg/L selenium group was lower than that of the control group. Different selenium concentrations had varying effects on BAK1 and APAF1 levels. APAF1 may play an important role in the pathogenesis of KBD. APAF1-related apoptosis was more pronounced in the middle and deep zones of the KBD cartilage. APAF may represent a potentially novel molecular target, which may be a biomarker of the role of selenium on the prevention and treatment of KBD. The role of BAK1 in the pathogenesis of KBD requires further study. Keywords Selenium Apoptosis signalling pathway Chondrocyte APAF1 BAK1 Kashin–Beck disease (KBD)