期刊文献+

Caveolin-1 Re-Expression Reverses G_0/G_1 Arrest in Caveolin-1 Knockout Mesangial Cells

Caveolin-1 Re-Expression Reverses G_0/G_1 Arrest in Caveolin-1 Knockout Mesangial Cells
原文传递
导出
摘要 Flow cytometry,BrdU incorporation,and western blotting were used to investigate whether caveolin-1(Cav-1) is involved in cell cycle progression of renal glomerular mesangial cells.Wide type mesangial cells re-entered the cell cycle after 22 h incubation with 20% fetal bovine serum(FBS) and Cav-1 knockout cells remained in G0/G1 phase after 48 h,which indicated that Cav-1 knockout mesangial cells were G0/G1 arrest.The protein level of cyclin D1 significantly increased after incubation with 20% FBS for 6 h in wide type mesangial cells,and 12 h in Cav-1 knockout cells.It suggested that cyclin D1 upregulation was delayed in knockout mesangial cells.Cav-1 re-expression in Cav-1 knockout mesangial cells increased the ratio of S phase from 4.8% to 15.26%,and decreased the ratio of G0/G1 phase from 90.96% to 77.84%,which implied that Cav-1 re-expression can reverse cell cycle arrest.It concludes that Cav-1 may promote the proliferation of mesangial cells. Flow cytometry,BrdU incorporation,and western blotting were used to investigate whether caveolin-1(Cav-1) is involved in cell cycle progression of renal glomerular mesangial cells.Wide type mesangial cells re-entered the cell cycle after 22 h incubation with 20% fetal bovine serum(FBS) and Cav-1 knockout cells remained in G0/G1 phase after 48 h,which indicated that Cav-1 knockout mesangial cells were G0/G1 arrest.The protein level of cyclin D1 significantly increased after incubation with 20% FBS for 6 h in wide type mesangial cells,and 12 h in Cav-1 knockout cells.It suggested that cyclin D1 upregulation was delayed in knockout mesangial cells.Cav-1 re-expression in Cav-1 knockout mesangial cells increased the ratio of S phase from 4.8% to 15.26%,and decreased the ratio of G0/G1 phase from 90.96% to 77.84%,which implied that Cav-1 re-expression can reverse cell cycle arrest.It concludes that Cav-1 may promote the proliferation of mesangial cells.
出处 《Wuhan University Journal of Natural Sciences》 CAS 2010年第6期532-538,共7页 武汉大学学报(自然科学英文版)
基金 Supported by the National Natural Science Foundation of China (30700370)
关键词 肾小球系膜细胞 基因敲除 小窝 WESTERN印迹 细胞周期阻滞 G1期阻滞 cyclin 胎牛血清 mesangial cell caveolin-1(Cav-1) knockout cell cycle arrest diabetic nephropathy
  • 相关文献

参考文献28

  • 1Parat M O. The biology of caveolae: Achievements and perspectives [J]. Int Rev Cell Mol Biol, 2009, 273:117-162.
  • 2Chidlow J H Jr, Sessa W C. Caveolae, caveolins, and cavins: Complex control of cellular signalling and inflammation [J]. Cardiovasc Res, 2010, 86(2): 219-225.
  • 3Doherty G J, McMahon H T. Mechanisms of endocytosis [J]. Annu Rev Biochem, 2009, 78: 857-902.
  • 4von Eckardstein A, Rohrer L. Transendothelial lipoprotein transport and regulation of endothelial permeability and integrity by lipoproteins [J]. Curt Opin Lipidol, 2009, 20(3): 197-205.
  • 5Frank P G, Hassan G S, Rodriguez-Feo J A,et al. Caveolae and caveolin-1: Novel potential targets for the treatment of cardiovascular disease [J]. Curr Pharm Des, 2007, 13(17): 1761-1769.
  • 6Yin X, Li B, Chen H, et al. Differential signaling pathways in angiotensin II- and epidermal growth factor-stimulated hepatic C9 cells [J]. Mol Pharmaco, 2008, 74(5): 1223-1233.
  • 7Ushio-Fukai M, Zuo L, Ikeda S, et al. cAbl tyrosine kinase mediates reactive oxygen species- and caveolin-dependent AT1 receptor signaling in vascular smooth muscle: role in vascular hypertrophy [J]. Cire Res, 2005, 97(8): 829-836.
  • 8Williams T M, Lisanti M E The Caveolin genes: From cell biology to medicine [J]. Ann Med, 2004, 36(8): 584-595.
  • 9Schwencke C, Braun-Dullaeus R C, Wunderlich C, et al. Caveolae and caveolin in transmembrane signaling: Implications for human disease [J]. Cardiovasc Res, 2006, 70(1): 42-49.
  • 10Cerezo A, Guadamillas M C, Goetz J G, et al. The absence of caveolin-1 increases proliferation and anchorage-independent growth by a Rac-dependent, Erk-independent mechanism [J]. Mol Cell Biol, 2009, 29(18): 5046-5059.

二级参考文献12

  • 1Bartus R T,Dean R L,Beer B,et al.The Cholinergic Hypothesis of Geriatric Memory Dysfunction. Science . 1982
  • 2Benzi G,Moretti A.Is There a Rationale for the Use of Acetylcholinesterase Inhibitors in the Therapy of Alzheimer’ s disease. European Journal of Pharmacology . 1998
  • 3Choi D W,Koh J Y,Peters S.Pharmacology of Glutamate Neurotoxicity in Cortical Cell Culture: Attenuation by NMDA Antagonists. The Journal of Neuroscience . 1988
  • 4Hershkowitz N,Rogawski M A.Tetrahydroaminoacridine Block of N-methyl -D-Aspartate-Activated Cation Channels in Cultured Hippocampal Neurons. Molecular Pharmacology . 1991
  • 5Pang Y P,Quiram P,Jelacic T,et al.Highly Potent ,Selective, and Low Cost bis-Tetrahydroaminoacrine Inhibitors of Acetylcholinesterase. Journal of Biological Chemistry . 1996
  • 6Marvizon J C,Lewin A H,Skolnick P.1-Aminocyclopropane Carboxylic Acid: a Potent and Selective Ligand for the Glycine Modulatory Site of the Nmethyl -D-Aspartate Receptor Complex. Journal of Neurochemistry . 1989
  • 7Davenport C J,Monyer H Choi D W.Tetrahydroaminoacridine Selectively Attenuates NMDA Receptor -Mediated Neurotoxicity. European Journal of Pharmacology . 1988
  • 8Albin R L,Young A B,Penney J B.Tetrahydro-9Aminoacridine ( THA) Interacts with the Phencyclidine (PCP) Receptor Site. Neuroscience Letters . 1988
  • 9Holscher C.Possible Causes of Alzheimer’ s disease:Amyloid Fragments, Free Radicals, and Calcium Homeostasis. Neurobiology of Disease . 1998
  • 10Lipton S A,Rosenberg P A.Excitatory Amino Acids as a Final Common pathway for Neurologic Disorders. The New England Journal of Medicine . 1994

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部