Podocyte biology in diabetic nephropathy

Kidney International

Volumn 72, Issue SUPPL. 106, 2007, Pages

  Li, J J ^a,b   Kwak, S J ^b   Jung, D S ^b   Kim, J J ^b   Yoo, T H ^b   Ryu, D R ^c   Han, S H ^b   Choi, H Y ^b   Lee, J E ^b   Moon, S J ^b   Kim, D K ^b   Han, D S ^b   Kang, S W ^b  

^a YANBIAN UNIVERSITY MEDICAL COLLEGE   (China)

^b Yonsei University College of Medicine   (South Korea)

^c Ewha Womans University School of Medicine   (South Korea)

Author keywords

Diabetic nephropathy; Foot process effacement; Glomerulosclerosis; Hypertrophy; Podocyte; Podocytopenia

Indexed keywords

ANGIOTENSIN 1 RECEPTOR ANTAGONIST;

CELL DAMAGE; CELL FUNCTION; CELL STRUCTURE; CONFERENCE PAPER; CYTOLOGY; DIABETIC NEPHROPATHY; FOOT PROCESS EFFACEMENT; GLOMERULAR HYPERTROPHY; GLOMERULOPATHY; GLOMERULOSCLEROSIS; KIDNEY DISEASE; NONHUMAN; PODOCYTE; PODOCYTOPENIA; PRIORITY JOURNAL; CELL JUNCTION; CELL PROLIFERATION; DISEASE COURSE; GLOMERULUS; HUMAN; HYPERTROPHY; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY; REVIEW;

CELL PROLIFERATION; DIABETIC NEPHROPATHIES; DISEASE PROGRESSION; HUMANS; HYPERTROPHY; INTERCELLULAR JUNCTIONS; KIDNEY GLOMERULUS; PODOCYTES;

EID: 34547467760     PISSN: 00852538     EISSN: 15231755     Source Type: Journal    
DOI: 10.1038/sj.ki.5002384     Document Type: Conference Paper

References (88)

1. Pavenstadt H, Kriz W, Kretzler M. Cell biology of the glomerular podocyte. Physiol Rev 2003; 83: 253-307.
2. Tryggvason K, Wartiovaara J. Molecular basis of glomerular permselectivity. Curr Opin Nephrol Hypertens 2001; 10: 543-549.
3. Shankland SJ. The podocyte's response to injury: role in proteinuria and glomerulosclerosis. Kidney Int 2006; 69: 2131-2147.
4. United States Renal Data System 2005 Annual Data Report. Incidence & prevalence. Am J Kidney Dis 2006; 47(Suppl 1): 65-80.
5. European Dialysis Transplant Association. Report on management of renal failure in Europe, XXVI, 1995. Nephrol Dial Transplant 1996; 11(Suppl 7): 1-32.
6. Wolf G, Chen S, Ziyadeh FN. From the periphery of the glomerular capillary wall toward the center of disease: podocyte injury comes of age in diabetic nephropathy. Diabetes 2005; 54: 1626-1634.
7. Baumgartl HJ, Sigl G, Banholzer P et al. On the prognosis of IDDM patients with larger kidneys. Nephrol Dial Transplant 1998; 13: 630-634.
8. Wolf G, Ziyadeh FN. Molecular mechanisms of diabetic renal hypertrophy. Kidney Int 1999; 56: 393-405.
9. Young BA, Johnson RJ, Alpers CE et al. Cellular events in the evolution of experimental diabetic nephropathy. Kidney Int 1995; 47: 935-944.
10. Wolf G. Cell cycle regulation in diabetic nephropathy. Kidney Int 2000; 58(Suppl 77): S59-S66.
11. King RW, Jackson PK, Kirschner MW. Mitosis in transition. Cell 1994; 79: 563-571.
12. Liu B, Preisig PA. TGF-β1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase. Am J Physiol 1999; 277: F186-F194.
13. Sherr CJ, Roberts JM. Inhibitors of mammalian G1 cyclin-dependent kinases. Genes Dev 1995; 9: 1149-1163.
14. Harper JW, Adami GR, Wei N et al. The p21 Cdk-interacting protein Cip1 is a potent inhibitor of G1 cyclin- dependent kinases. Cell 1993; 75: 805-816.
15. Kip1, a cyclin-Cdk inhibitor, links transforming growth factor-β and contact inhibition to cell cycle arrest. Genes Dev 1994; 8: 9-22.
16. 27Kip1 in cultured mouse mesangial cells: relationship to hypertrophy. Am J Physiol 1997; 273: 348-356.
17. Kip1 in diabetic db/db mouse: role of hyperglycemia. Kidney Int 1998; 53: 869-879.
18. Kip1 expression in diabetic BBdp rats. Diabetologia 1999; 42: 1425-1432.
19. WAF1,CIP1 is increased in experimental diabetic nephropathy: potential role in glomerular hypertrophy. J Am Soc Nephrol 1998; 9: 986-993.
20. Barisoni L, Kriz W, Mundel P, D'Agati V. The dysregulated podocyte phenotype: a novel concept in the pathogenesis of collapsing idiopathic focal segmental glomerulosclerosis and HIV-associated nephropathy. J Am Soc Nephrol 1999; 10: 51-61.
21. Nagata M, Hattori M, Hamano Y et al. Origin and phenotypic features of hyperplastic epithelial cells in collapsing glomerulopathy. Am J Kidney Dis 1998; 32: 962-969.
22. D'Agati V. The many masks of focal segmental glomerulosclerosis. Kidney Int 1994; 46: 1223-1241.
23. Petermann AT, Pippin J, Durvasula R et al. Mechanical stretch induces podocyte hypertrophy in vitro. Kidney Int 2005; 67: 157-166.
24. Kip1 expression in glucose-stimulated podocytes and in diabetic glomeruli. Kidney Int 2005; 67: 944-952.
25. Yoo TH, Li JJ, Kim JJ et al. Local renin-angiotensin system is activated in podocytes under diabetic conditions. Kidney Int (in submission).
26. Mason RM, Wahab NA. Extracellular matrix metabolism in diabetic nephropathy. J Am Soc Nephrol 2003; 14: 1358-1373.
27. Zhu D, Kim Y, Steffes MW et al. Glomerular distribution of type IV collagen in diabetes by high resolution quantitative immunochemistry. Kidney Int 1994; 45: 425-433.
28. Yagame M, Kim Y, Zhu D et al. Differential distribution of type IV collagen chains in patients with diabetic nephropathy in non-insulin-dependent diabetes mellitus. Nephron 1995; 70: 42-48.
29. Zeisberg M, Ericksen MB, Hamano Y et al. Differential expression of type IV collagen isoforms in rat glomerular endothelial and mesangial cells. Biochem Biophys Res Commun 2002; 295: 401-407.
30. Shimomura H, Spiro RG. Studies on macromolecular components of human glomerular basement membrane and alterations in diabetes. Decreased levels of heparan sulfate proteoglycans and laminin. Diabetes 1987; 36: 374-381.
31. Iglesias-de la Cruz MC, Ziyadeh FN et al. Effects of high glucose and TGF-β1 on the expression of collagen IV and vascular endothelial growth factor in mouse podocytes. Kidney Int 2002; 62: 901-913.
32. Kang SW, Natarajan R, Shahed A et al. Role of 12-lipoxygenase in the stimulation of p38 mitogen-activated protein kinase and collagen α5(IV) in experimental diabetic nephropathy and in glucose-stimulated podocytes. J Am Soc Nephrol 2003; 14: 3178-3187.
33. Bai Y, Wang L, Li Y et al. High ambient glucose levels modulates the production of MMP-9 and α5(IV) collagen by cultured podocytes. Cell Physiol Biochem 2006; 17: 57-68.
34. Chen S, Lee JS, Iglesias-de la Cruz MC et al. Angiotensin II stimulates α3(IV) collagen production in mouse podocytes via TGF-β and VEGF signalling: implications for diabetic glomerulopathy. Nephrol Dial Transplant 2005; 20: 1320-1328.
35. Ayo SH, Radnik RA, Glass WF II et al. Increased extracellular matrix synthesis and mRNA in mesangial cells grown in high-glucose medium. Am J Physiol 1991; 260: F185-F191.
36. Kitamura M, Kitamura A, Mitarai T et al. Gene expression of metalloproteinase and its inhibitor in mesangial cells exposed to high glucose. Biochem Biophys Res Commun 1992; 185: 1048-1054.
37. Steffes MW, Schmidt D, McCrery R, Basgen JM. Glomerular cell number in normal subjects and in type 1 diabetic patients. Kidney Int 2001; 59: 2104-2113.
38. Pagtalunan ME, Miller PL, Jumping-Eagle S et al. Podocyte loss and progressive glomerular injury in type II diabetes. J Clin Invest 1997; 99: 342-348.
39. Regoli M, Bendayan M. Alterations in the expression of the α3β1 integrin in certain membrane domains of the glomerular epithelial cells (podocytes) in diabetes mellitus. Diabetologia 1997; 40: 15-22.
40. Chen HC, Chen CA, Guh JY et al. Altering expression of α3β1 integrin on podocytes of human and rats with diabetes. Life Sci 2000; 67: 2345-2353.
41. Kitsiou PV, Tzinia AK, Stetler-Stevenson WG et al. Glucose-induced changes in integrins and matrix-related functions in cultured human glomerular epithelial cells. Am J Physiol Renal Physiol 2003; 284: F671-F679.
42. Han SY, Kang YS, Jee YH et al. High glucose and angiotensin II increase b1 integrin and integrin-linked kinase synthesis in cultured mouse podocytes. Cell Tissue Res 2006; 323: 321-332.
43. Dedhar S, Williams B, Hannigan G. Integrin-linked kinase (ILK): a regulator of integrin and growth-factor signalling. Trends Cell Biol 1999; 9: 319-323.
44. Schiffer M, Bitzer M, Roberts IS et al. Apoptosis in podocytes induced by TGF-β and Smad7. J Clin Invest 2001; 108: 807-816.
45. Wada T, Pippin JW, Terada Y, Shankland SJ. The cyclin-dependent kinase inhibitor p21 is required for TGF-β1-induced podocyte apoptosis. Kidney Int 2005; 68: 1618-1629.
46. Durvasula RV, Petermann AT, Hiromura K et al. Activation of a local tissue angiotensin system in podocytes by mechanical strain. Kidney Int 2004; 65: 30-39.
47. Susztak K, Raff AC, Schiffer M, Bottinger EP. Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy. Diabetes 2006; 55: 225-233.
48. Kriz W, Gretz N, Lemley KV. Progression of glomerular diseases: is the podocyte the culprit? Kidney Int 1998; 54: 687-697.
49. Mundel P, Shankland SJ. Podocyte biology and response to injury. J Am Soc Nephrol 2002; 13: 3005-3015.
50. Kestila M, Lenkkeri U, Mannikko M et al. Positionally cloned gene for a novel glomerular protein-nephrin is mutated in congenital nephrotic syndrome. Mol Cell 1998; 1: 575-582.
51. Ruotsalainen V, Ljungberg P, Wartiovaara J et al. Nephrin is specifically located at the slit diaphragm of glomerular podocytes. Proc Natl Acad Sci USA 1999; 96: 7962-7967.
52. Donoviel DB, Freed DD, Vogel H et al. Proteinuria and perinatal lethality in mice lacking NEPH1, a novel protein with homology to NEPHRIN. Mol Cell Biol 2001; 21: 4829-4836.
53. Reiser J, Kriz W, Kretzler M, Mundel P. The glomerular slit diaphragm is a modified adherens junction. J Am Soc Nephrol 2000; 11: 1-8.
54. Inoue T, Yaoita E, Kurihara H et al. FAT is a component of glomerular slit diaphragms. Kidney Int 2001; 59: 1003-1012.
55. Shih NY, Li J, Cotran R et al. CD2AP localizes to the slit diaphragm and binds to nephrin via a novel C-terminal domain. Am J Pathol 2001; 159: 2303-2308.
56. Schwarz K, Simons M, Reiser J et al. Podocin, a raft-associated component of the glomerular slit diaphragm, interacts with CD2AP and nephrin. J Clin Invest 2001; 108: 1621-1629.
57. Kurihara H, Anderson JM, Farquhar MG. Diversity among tight junctions in rat kidney: glomerular slit diaphragms and endothelial junctions express only one isoform of the tight junction protein ZO-1. Proc Natl Acad Sci USA 1992; 89: 7075-7079.
58. Boute N, Roselli S, Benessy F et al. NPHS2 encoding the glomerular proteins podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome. Nat Genet 2000; 24: 349-354.
59. Kim JM, Wu H, Green G et al. CD2-associated protein haploinsufficiency is linked to glomerular disease susceptibility. Science 2003; 300: 1298-1300.
60. Shih NY, Li J, Karpitskii V et al. Congenital nephrotic syndrome in mice lacking CD2-associated protein. Science 1999; 286: 312-315.
61. Putaala H, Soininen R, Kilpelainen P et al. The murine nephrin gene is specifically expressed in kidney, brain and pancreas: Inactivation of the gene leads to massive proteinuria and neonatal death. Hum Mol Genet 2001; 10: 1-8.
62. Bonnet F, Cooper ME, Kawachi H et al. Irbesartan normalises the deficiency in glomerular nephrin expression in a model of diabetes and hypertension. Diabetologia 2001; 44: 874-877.
63. Doublier S, Salvidio G, Lucia E et al. Nephrin expression is reduced in human diabetic nephropathy: evidence for a distinct role for glycated albumin and angiotensin II. Diabetes 2003; 52: 1023-1030.
64. Menne J, Meier M, Park JK et al. Nephrin loss in experimental diabetic nephropathy is prevented by deletion of protein kinase C a signaling in-vivo. Kidney Int 2006; 70: 1456-1462.
65. Langham RG, Kelly DJ, Cox AJ et al. Proteinuria and the expression of the podocyte slit diaphragm protein, nephrin, in diabetic nephropathy: effects of angiotensin converting enzyme inhibition. Diabetologia 2002; 45: 1572-1576.
66. Aaltonen P, Luimula P, Astrom E et al. Changes in the expression of nephrin gene and protein in experimental diabetic nephropathy. Lab Invest 2001; 81: 1185-1190.
67. Sung SH, Ziyadeh FN, Wang A et al. Blockade of vascular endothelial growth factor signaling ameliorates diabetic albuminuria in mice. J Am Soc Nephrol 2006; 17: 3093-3104.
68. Langham RG, Kelly DJ, Cox AJ et al. Angiotensin II-induced proteinuria and expression of the podocyte slit pore membrane protein, nephrin. Nephrol Dial Transplant 2004; 19: 262-263.
69. Xu ZG, Ryu DR, Yoo TH et al. P-Cadherin is decreased in diabetic glomeruli and in glucose-stimulated podocytes in vivo and in vitro studies. Nephrol Dial Transplant 2005; 20: 524-531.
70. Rincon-Choles H, Vasylyeva TL, Pergola PE et al. ZO-1 expression and phosphorylation in diabetic nephropathy. Diabetes 2006; 55: 894-900.
71. Koop K, Eikmans M, Baelde HJ et al. Expression of podocyte-associated molecules in acquired human kidney diseases. J Am Soc Nephrol 2003; 14: 2063-2071.
72. Benigni A, Gagliardini E, Tomasoni S et al. Selective impairment of gene expression and assembly of nephrin in human diabetic nephropathy. Kidney Int 2004; 65: 2193-2200.
73. Adler S, Chen X. Anti-Fx1A antibody recognizes a β1-integrin on glomerluar epithelial cells and inhibits adhesion and growth. Am J Physiol 1992; 262: F770-F776.
74. Kriedberg JA, Donovan MJ, Goldstein SL et al. 3β1 integrin has a crucial role in kidney and lung organogenesis. Development 1996; 122: 3537-3547.
75. Kojima K, Kerjaschki D. Is podocyte shape controlled by the dystroglycan complex? Nephrol Dial Transplant 2002; 17(Suppl 9): 23-24.
76. Raats CJ, van den Born J, Bakker MA et al. Expression of agrin, dystroglycan, and utrophin in normal renal tissue and in experimental glomerulopathies. Am J Pathol 2000; 156: 1749-1765.
77. Regele HM, Fillipovic E, Langer B et al. Glomerular expression of dystroglycans is reduced in minimal change nephrosis but not in focal segmental glomerulosclerosis. J Am Soc Nephrol 2000; 11: 403-412.
78. Makino H, Miyamoto Y, Sawai K et al. Altered gene expression related to glomerulogenesis and podocyte structure in early diabetic nephropathy of db/db mice and its restoration by pioglitazone. Diabetes 2006; 55: 2747-2756.
79. Dai T, Natarajan R, Nast CC et al. Glucose and diabetes: effects on podocyte and glomerular p38MAPK, heat shock protein 25, and actin cytoskeleton. Kidney Int 2006; 69: 806-814.
80. Asanuma K, Yanagida-Asanuma E, Faul C et al. Synaptopodin orchestrates actin organization and cell motility via regulation of RhoA signalling. Nat Cell Biol 2006; 8: 485-491.
81. Etienne-Manneville S, Hall A. Rho GTPases in cell biology. Nature 2002; 420: 629-635.
82. Asanuma K, Kim K, Oh J et al. Synaptopodin regulates the actin-bundling activity of alpha-actinin in an isoform-specific manner. J Clin Invest 2005; 115: 1188-1198.
83. Blanco S, Bonet J, Lopez D et al. ACE inhibitors improve nephrin expression in Zucker rats with glomerulosclerosis. Kidney Int 2005; 67(Suppl 93): S10-S14.
84. Takeda T, McQuistan T, Orlando RA, Farquhar MG. Loss of glomerular foot processes is associated with uncoupling of podocalyxin from the actin cytoskeleton. J Clin Invest 2001; 108: 289-301.
85. Doyonnas R, Kershaw D, Duhme C et al. Anuria, omphalocele, and perinatal lethality in mice lacking the CD-34 related protein podocalyxin. J Exp Med 2001; 94: 13-27.
86. Economou CG, Kitsiou PV, Tzinia AK et al. Enhanced podocalyxin expression alters the structure of podocyte basal surface. J Cell Sci 2004; 117: 3281-3294.
87. Breiteneder-Geleff S, Matsui K, Soleiman A et al. Podoplanin, novel 43-kd membrane protein of glomerular epithelial cells, is down-regulated in puromycin nephrosis. Am J Pathol 1997; 151: 1141-1152.
88. Matsui K, Breiteneder-Geleff S, Kerjaschki D. Epitope-specific antibodies to the 43-kD glomerular membrane protein podoplanin cause proteinuria and rapid flattening of podocytes. J Am Soc Nephrol 1998; 9: 2013-2026.