Advanced glycation end products promote proliferation and suppress autophagy via reduction of Cathepsin D in rat vascular smooth muscle cells

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• 作者：Mingfeng Ma (1) (2)
  Xiaofan Guo (1)
  Ye Chang (1)
  Chao Li (3)
  Xin Meng (3)
  Si Li (4)
  Zhen-Xian Du (4)
  Hua-Qin Wang (3)
  Yingxian Sun (1)
  
  1. Department of Cardiology ; The First Hospital of China Medical University ; 155 Nanjing North Street ; Heping District ; Shenyang ; 110001 ; Liaoning ; People鈥檚 Republic of China
  2. Department of Cardiology ; Fenyang hospital of shanxi province ; Fenyang ; Shanxi ; People鈥檚 Republic of China
  3. Department of Biochemistry and Molecular Biology ; China Medical University ; Shenyang ; Liaoning ; People鈥檚 Republic of China
  4. Department of Endocrinology and Metabolism ; The First Hospital of China Medical University ; Shenyang ; Liaoning ; People鈥檚 Republic of China
  
• 关键词：Diabetic vascular complication ; Advanced glycation end products (AGEs) ; Cathepsin D (CatD) ; Autophagy ; Phenotypic modulation ; Vascular smooth muscle cells (VSMCs)
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2015
• 出版时间：May 2015
• 年：2015
• 卷：403
• 期：1-2
• 页码：73-83
• 全文大小：3,903 KB
• 参考文献：1. Ammit, AJ, Panettieri, RA (2001) The circle of life: cell cycle regulation in airway smooth muscle. J Appl Physiol 91: pp. 1431-1437
  2. Kudryavtseva, O, Aalkjaer, C, Matchkov, VV (2013) Vascular smooth muscle cell phenotype is defined by Ca2+-dependent transcription factors. FEBS J 280: pp. 5488-5499 CrossRef
  3. Owens, GK, Kumar, MS, Wamhoff, BR (2004) Molecular regulation of vascular smooth muscle cell differentiation in development and disease. Physiol Rev 84: pp. 767-801 CrossRef
  4. House, SJ, Potier, M, Bisaillon, J, Singer, HA, Trebak, M (2008) The non-excitable smooth muscle: calcium signaling and phenotypic switching during vascular disease. Pflugers Arch 456: pp. 769-785 CrossRef
  5. Rzucidlo, EM, Martin, KA, Powell, RJ (2007) Regulation of vascular smooth muscle cell differentiation. J Vasc Surg 45: pp. A25-A32 CrossRef
  6. Orr, AW, Hastings, NE, Blackman, BR, Wamhoff, BR (2010) Complex regulation and function of the inflammatory smooth muscle cell phenotype in atherosclerosis. J Vasc Res 47: pp. 168-180 CrossRef
  7. Singh, R, Barden, A, Mori, T (2001) Advanced glycation end-products: a review. Diabetologia 44: pp. 129-146 CrossRef
  8. Hudson, BI, Schmidt, AM (2004) RAGE: a novel target for drug intervention in diabetic vascular disease. Pharm Res 21: pp. 1079-1086 CrossRef
  9. Vlassara, H (1996) Advanced glycation end-products and atherosclerosis. Ann Med 28: pp. 419-426 CrossRef
  10. Kilhovd, BK, Berg, TJ, Birkeland, KI, Thorsby, P, Hanssen, KF (1992) Serum levels of advanced glycation end products are increased in patients with type 2 diabetes and coronary heart disease. Diabetes Care 22: pp. 1543-1548 CrossRef
  11. Yamagishi, S, Matsui, T (2010) Smooth muscle cell pathophysiology and advanced glycation end products (AGEs). Curr Drug Targets 11: pp. 875-881 CrossRef
  12. Satoh, H, Togo, M, Hara, M, Miyata, T, Han, K, Maekawa, H, Ohno, M, Hashimoto, Y, Kurokawa, K, Watanabe, T (1997) Advanced glycation endproducts stimulate mitogen-activated protein kinase and proliferation in rabbit vascular smooth muscle cells. Biochem. Biophys. Res. Commun. 239: pp. 111-115 CrossRef
  13. David, KC, Scott, RH, Nixon, GF (2008) Advanced glycation endproducts induce a proliferative response in vascular smooth muscle cells via altered calcium signaling. Biochem Pharmacol 76: pp. 1110-1120 CrossRef
  14. Reddy, MA, Li, SL, Sahar, S, Kim, YS, Xu, ZG, Lanting, L, Natarajan, R (2006) Key role of Src kinase in S100B-induced activation of the receptor for advanced glycation end products in vascular smooth muscle cells. J Biol Chem 281: pp. 13685-13693 CrossRef
  15. Ravikumar, B, Sarkar, S, Davies, JE, Futter, M, Garcia-Arencibia, M (2010) Regulation of mammalian autophagy in physiology and pathophysiology. Physiol Rev 90: pp. 1383-1435 CrossRef
  16. Mizushima, N, Komatsu, M (2011) Autophagy: renovation of cells and tissues. Cell 147: pp. 728-741 CrossRef
  17. Salabei, JK, Hill, BG (2013) Implications of autophagy for vascular smooth muscle cell function and plasticity. Free Radic Biol Med 65: pp. 693-703 CrossRef
  18. Hou, X, Hu, Z, Xu, H, Xu, J, Zhang, S, Zhong, Y, He, X, Wang, N (2014) Advanced glycation endproducts trigger autophagy in cadiomyocyte via RAGE/PI3K/AKT/mTOR pathway. Cardiovasc Diabetol 13: pp. 78 CrossRef
  19. Kaminura, M, Bea, F, Akizawa, T (2004) Platelet-derived growth factor induces tissue factor expression in vascular smooth muscle cells via activation of Egr-1. Hypertension 44: pp. 944-951 CrossRef
  20. Salabei, JK, Cummins, TD, Singh, M, Jones, SP, Bhatnagar, A, Hill, BG (2013) PDGF-mediated autophagy regulates vascular smooth muscle cell phenotype and resistance to oxidative stress. Biochem J 451: pp. 375-388 CrossRef
  21. Hou, FF, Chertow, GM, Kay, J (1997) Interaction between beta 2-microglobulin and advanced glycation end products in the development of dialysis related-amyloidosis. Kidney Int 51: pp. 1514-1519 CrossRef
  22. Yoshimori, T, YamamotoA, A, Moriyama, Y, Futai, M, Tashiro, Y (1991) Bafilomycin A1, a specific inhibitor of vacuolar-type H(+)-ATPase, inhibits acidification and protein degradation in lysosomes of cultured cells. J Biol Chem 266: pp. 17707-17712
  23. Salabei, JK, Cummins, TD, Singh, M, Jones, SP, Bhatnagar, A, Hill, BG (2013) PDGF-mediated autophagy regulates vascular smooth muscle cell phenotype and resistance to oxidative stress. Biochem J 451: pp. 375-388 CrossRef
  24. Hu, P, Lai, D, Lu, P, Gao, J, He, H (2012) ERK and Akt signaling pathways are involved in advanced glycation end product-induced autophagy in rat vascular smooth muscle cells. Int J Mol Med 29: pp. 613-618
  25. Toure, F, Fritz, G, Li, Q, Rai, V, Daffu, G, Zou, YS, Rosario, R, Ramasamy, R, Alberts, AS, Yan, SF, Schmidt, AM (2012) Formin mDia1 mediates vascular remodeling via integration of oxidative and signal transduction pathways. Circ Res 110: pp. 1279-1293 CrossRef
  26. Zhao, LM, Su, XL, Wang, Y, Li, GR, Deng, XL (2013) KCa3.1 channels mediate the increase of cell migration and proliferation by advanced glycation endproducts in cultured rat vascular smooth muscle cells. Lab Invest 93: pp. 159-167 CrossRef
  27. Chung, TW, Choi, HJ, Kim, CH, Jeong, HS (1833) Ha KT (2013) Lipocalin-2 elicited by advanced glycation end-products promotes the migration of vascular smooth muscle cells. Biochim Biophys Acta 12: pp. 3386-3395
  28. San Martin, A, Foncea, R, Laurindo, FR, Ebensperger, R, Griendling, KK, Leighton, F (2007) Nox1-based NADPH oxidase-derived superoxide is required for VSMC activation by advanced glycation end-products. Free Radic Biol Med 42: pp. 1671-1679 CrossRef
  29. Yan, SF, Ramasamy, R, Schmidt, AM (2009) Receptor for AGE (RAGE) and its ligands-cast into leading roles in diabetes and the inflammatory response. J Mol Med (Berl) 87: pp. 235-247 CrossRef
  30. Aronson, D (2002) Potential role of advanced glycosylation end products in promoting restenosis in diabetes and renal failure. Med Hypotheses 59: pp. 297-301 CrossRef
  31. Jia, G, Cheng, G, Agrawal, DK (2007) Autophagy of vascular smooth muscle cells in atherosclerotic lesions. Autophagy 3: pp. 63-64 CrossRef
  32. Martinet, W, Meyer, GR (2008) Autophagy in atherosclerosis. Curr Atheroscler Rep 10: pp. 216-223 CrossRef
  33. Turk, B, Stoka, V, Rozman-Pungercar, J, Cirman, T, Droga-Mazovec, G, Oresi膰, K, Turk, V (2002) Apoptotic pathways: involvement of lysosomal proteases. Biol Chem 383: pp. 1035-1044
  34. Punnonen, EL, Autio, S, Marjom盲ki, VS, Reunanen, H (1992) Autophagy, cathepsin L transport, and acidification in cultured rat fibroblasts. J Histochem Cytochem 40: pp. 1579-1587 CrossRef
  35. Uchiyama, Y (2001) Autophagic cell death and its execution by lysosomal cathepsins. Arch Histol Cytol 64: pp. 233-246 CrossRef
  36. Tatti, M, Motta, M, Bartolomeo, S, Cianfanelli, V, Salvioli, R (2013) Cathepsin-mediated regulation of autophagy in saposin C deficiency. Autophagy 9: pp. 241-243 CrossRef
  37. Kute, TE, Russell, GB, Zbieranski, N, Long, R, Johnston, S, Williams, H, Stackhouse, C, Wilkins, L, Evans, I, Berry, P, Rimmer, K, Tucker, E (2004) Prognostic markers in node-negative breast cancer: a prospective study. Cytometry B Clin Cytom 59: pp. 24-31 CrossRef
  38. Hu, L, Roth, JM, Brooks, P, Luty, J, Karpatkin, S (2008) Thrombin up-regulates cathepsin D which enhances angiogenesis, growth, and metastasis. Cancer Res 68: pp. 4666-4673 CrossRef
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Life Sciences
  Biochemistry
  Medical Biochemistry
  Oncology
  Cardiology
  
• 出版者：Springer Netherlands
• ISSN：1573-4919

文摘

Autophagy is closely involved in vascular smooth muscle cell (VSMC) function, but little is known about the association between advanced glycation end products (AGEs) and autophagy and its role in AGEs-induced proliferation and migration of VSMCs. The current study investigated the effects of AGEs on the phenotypic modulation and autophagy of VSMCs, as well as the potential underlying mechanisms. Primary rat VSMCs were treated with bovine serum albumin or AGEs. Cell proliferation was detected by MTT assay, real-time cell analyzer and EdU incorporation. Cell cycle was analyzed by Hoechst staining and flow cytometry. The migration of VSMCs was detected by wound-healing assay and transwell migration assay. LC3 transition and p62 accumulation were detected using Western blotting. Acidic vacuoles were measured using AO and MDC staining. Cathepsin D (CatD) was transduced to VSMCs via lentiviral vectors. AGEs enhanced proliferation and migration of primary rat VSMC in a time-dependent manner. AGEs significantly increased LC3-II transition and p62 expression, as well as accumulation of acidic vacuole, which was not further increased by bafilomycin A1. AGEs decreased CatD expression in a time-dependent pattern, and overexpression of CatD prohibited autophagy attenuation mediated by AGEs. CatD overexpression suppressed AGEs-induced proliferation of VSMCs. Nevertheless, CatD exhibited no effects on AGEs-induced migration of VSMCs. AGEs promote proliferation of VSMCs and suppress autophagy, at least in part via CatD reduction.