Stuart Shankland

Summary

Affiliation: University of Washington
Country: USA

Publications

  1. pmc Podocyte repopulation by renal progenitor cells following glucocorticoids treatment in experimental FSGS
    Jiong Zhang
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Seattle, WA 98195, USA
    Am J Physiol Renal Physiol 304:F1375-89. 2013
  2. pmc Both cyclin I and p35 are required for maximal survival benefit of cyclin-dependent kinase 5 in kidney podocytes
    Yoshinori Taniguchi
    Division of Nephrology, Department of Medicine, University of Washington, Seattle, WA 98195 6521, USA
    Am J Physiol Renal Physiol 302:F1161-71. 2012
  3. pmc De novo expression of podocyte proteins in parietal epithelial cells in experimental aging nephropathy
    Jiong Zhang
    Div of Nephrology, Dept of Medicine, Univ of Washington School of Medicine, Seattle, WA 98195 6521, USA
    Am J Physiol Renal Physiol 302:F571-80. 2012
  4. ncbi request reprint Cell cycle regulatory proteins in glomerular disease
    S J Shankland
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, Wash 98195 6521, USA
    Exp Nephrol 7:207-11. 1999
  5. ncbi request reprint Podocyte proliferation and differentiation in glomerular disease: role of cell-cycle regulatory proteins
    Sian V Griffin
    Division of Nephrology, University of Washington Medical Center, Seattle, WA 98195, USA
    Nephrol Dial Transplant 18:vi8-13. 2003
  6. ncbi request reprint The podocyte's response to injury: role in proteinuria and glomerulosclerosis
    S J Shankland
    Department of Medicine, Division of Nephrology, University of Washington, Seattle, Washington 98195, USA
    Kidney Int 69:2131-47. 2006
  7. ncbi request reprint Mesangial cell proliferation mediated by PDGF and bFGF is determined by levels of the cyclin kinase inhibitor p27Kip1
    S J Shankland
    Department of Nephrology, University of Washington, Seattle 98195, USA
    Kidney Int 51:1088-99. 1997
  8. ncbi request reprint Cyclin kinase inhibitors are increased during experimental membranous nephropathy: potential role in limiting glomerular epithelial cell proliferation in vivo
    S J Shankland
    Department of Nephrology, University of Washington, Seattle, USA
    Kidney Int 52:404-13. 1997
  9. ncbi request reprint TGF-beta in glomerular disease
    S J Shankland
    Department of Medicine, University of Washington, Seattle 98195, USA
    Miner Electrolyte Metab 24:168-73. 1998
  10. ncbi request reprint Cell cycle regulatory proteins in glomerular disease
    S J Shankland
    Division of Nephrology, University of Washington, Seattle 98195, USA
    Kidney Int 56:1208-15. 1999

Research Grants

  1. Cell Cycle and Podocyte Apoptosis
    Stuart Shankland; Fiscal Year: 2009
  2. Cell Cycle and Podocyte Apoptosis
    Stuart Shankland; Fiscal Year: 2007
  3. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2003
  4. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2002
  5. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2001
  6. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2000
  7. Cell Cycle and Podocyte Apoptosis
    Stuart Shankland; Fiscal Year: 2009
  8. 6th International Podocyte Conference
    Stuart Shankland; Fiscal Year: 2006
  9. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2005
  10. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2007

Collaborators

Detail Information

Publications70

  1. pmc Podocyte repopulation by renal progenitor cells following glucocorticoids treatment in experimental FSGS
    Jiong Zhang
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Seattle, WA 98195, USA
    Am J Physiol Renal Physiol 304:F1375-89. 2013
    ..Prednisone limits podocyte loss by reducing apoptosis, and it increases regeneration by augmenting the number of podocyte progenitors. The data support a direct glomerular cell action for prednisone in improving outcomes in FSGS...
  2. pmc Both cyclin I and p35 are required for maximal survival benefit of cyclin-dependent kinase 5 in kidney podocytes
    Yoshinori Taniguchi
    Division of Nephrology, Department of Medicine, University of Washington, Seattle, WA 98195 6521, USA
    Am J Physiol Renal Physiol 302:F1161-71. 2012
    ..The results demonstrate that the activators of Cdk5, p35, and cyclin I are not required for normal kidney function. However, they play pivotal coordinated roles in maintaining podocyte survival during stress states in disease...
  3. pmc De novo expression of podocyte proteins in parietal epithelial cells in experimental aging nephropathy
    Jiong Zhang
    Div of Nephrology, Dept of Medicine, Univ of Washington School of Medicine, Seattle, WA 98195 6521, USA
    Am J Physiol Renal Physiol 302:F571-80. 2012
    ..These results suggest that although the number of PECs and PECs expressing podocyte proteins increase in aging nephropathy, they are likely not sufficient to compensate for the decrease in podocyte number...
  4. ncbi request reprint Cell cycle regulatory proteins in glomerular disease
    S J Shankland
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, Wash 98195 6521, USA
    Exp Nephrol 7:207-11. 1999
    ..Thus, identifying specific cell cycle regulatory proteins following injury may provide future targets for therapy in glomerular disease...
  5. ncbi request reprint Podocyte proliferation and differentiation in glomerular disease: role of cell-cycle regulatory proteins
    Sian V Griffin
    Division of Nephrology, University of Washington Medical Center, Seattle, WA 98195, USA
    Nephrol Dial Transplant 18:vi8-13. 2003
    ..Current work is aimed at further delineating the mechanisms regulating podocyte proliferation...
  6. ncbi request reprint The podocyte's response to injury: role in proteinuria and glomerulosclerosis
    S J Shankland
    Department of Medicine, Division of Nephrology, University of Washington, Seattle, Washington 98195, USA
    Kidney Int 69:2131-47. 2006
    ..It is the hope that by delineating the events following injury to podocytes, therapies might be developed to reduce the burden of proteinuric renal diseases...
  7. ncbi request reprint Mesangial cell proliferation mediated by PDGF and bFGF is determined by levels of the cyclin kinase inhibitor p27Kip1
    S J Shankland
    Department of Nephrology, University of Washington, Seattle 98195, USA
    Kidney Int 51:1088-99. 1997
    ....
  8. ncbi request reprint Cyclin kinase inhibitors are increased during experimental membranous nephropathy: potential role in limiting glomerular epithelial cell proliferation in vivo
    S J Shankland
    Department of Nephrology, University of Washington, Seattle, USA
    Kidney Int 52:404-13. 1997
    ..Thus, changes in cell cycle regulatory proteins may regulate the response of GEC to injury and underlie the development of progressive glomerulosclerosis in diseases of the GEC...
  9. ncbi request reprint TGF-beta in glomerular disease
    S J Shankland
    Department of Medicine, University of Washington, Seattle 98195, USA
    Miner Electrolyte Metab 24:168-73. 1998
    ..However, TGF-beta may also have other important functions in the glomerulus, including the regulation of cell proliferation, hypertrophy, and survival (apoptosis), as well as modulation of the local and systemic immune response...
  10. ncbi request reprint Cell cycle regulatory proteins in glomerular disease
    S J Shankland
    Division of Nephrology, University of Washington, Seattle 98195, USA
    Kidney Int 56:1208-15. 1999
    ..Ultimately the goal is to find ever more appropriate therapeutic strategies to arrest or prevent progressive renal disease...
  11. ncbi request reprint Complement (C5b-9) induces glomerular epithelial cell DNA synthesis but not proliferation in vitro
    S J Shankland
    Department of Medicine, University of Washington, Seattle 98195, USA
    Kidney Int 56:538-48. 1999
    ..In the current study we determined if C5b-9 increases DNA synthesis in VEC in vitro, and defined the mechanisms involved...
  12. ncbi request reprint Podocyte expression of the CDK-inhibitor p57 during development and disease
    K Hiromura
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Kidney Int 60:2235-46. 2001
    ..Accordingly, we studied the role of the cyclin dependent kinase (CDK)-inhibitor p57Kip2 (p57) in modulating these processes...
  13. ncbi request reprint Cell cycle regulatory proteins in renal disease: role in hypertrophy, proliferation, and apoptosis
    S J Shankland
    Department of Medicine, Division of Nephrology, University of Washington Seattle, Washington 98195 6521, USA
    Am J Physiol Renal Physiol 278:F515-29. 2000
    ..With increasing understanding of the role for cell cycle regulatory proteins in renal disease comes the hope for potential therapeutic interventions...
  14. ncbi request reprint Activation of a local tissue angiotensin system in podocytes by mechanical strain
    Raghu V Durvasula
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Kidney Int 65:30-9. 2004
    ..Accordingly, we have tested the hypothesis that mechanical strain up-regulates local angiotensin II in podocytes, thereby resulting in a progressive reduction in podocyte number...
  15. pmc The enigmatic parietal epithelial cell is finally getting noticed: a review
    Takamoto Ohse
    Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195 6521, USA
    Kidney Int 76:1225-38. 2009
    ..The data show that PECs have unique properties and that new functions are being recognized such as their role in differentiating into podocytes during disease...
  16. ncbi request reprint Mechanical stress reduces podocyte proliferation in vitro
    Arndt T Petermann
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Kidney Int 61:40-50. 2002
    ..However, the effects of stretch on podocyte growth and the mechanisms that underlie this have not been elucidated...
  17. ncbi request reprint ATRA induces podocyte differentiation and alters nephrin and podocin expression in vitro and in vivo
    Michael R Vaughan
    Department of Medicine, Division of Nephrology, University of Washington, Seattle, Washington, USA
    Kidney Int 68:133-44. 2005
    ..The factors governing podocyte differentiation are poorly understood. We tested the hypothesis that all-trans retinoic acid (ATRA), a vitamin A derivative, induces podocyte differentiation in vitro and in vivo...
  18. ncbi request reprint Limitation of podocyte proliferation improves renal function in experimental crescentic glomerulonephritis
    Sian V Griffin
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Kidney Int 67:977-86. 2005
    ..The consequences of inhibiting podocyte proliferation on renal function have not been fully established. At the level of the cell cycle, cyclin-dependent kinase 2 (CDK2) is required for proliferation...
  19. ncbi request reprint Mechanical stretch induces podocyte hypertrophy in vitro
    Arndt T Petermann
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Kidney Int 67:157-66. 2005
    ..Increased intraglomerular pressure causes stress-tension, or stretch, on resident glomerular cells. However, the effects of stretch on podocyte growth, and the mechanisms that underlie this, have not been elucidated...
  20. ncbi request reprint The renin-angiotensin system in glomerular podocytes: mediator of glomerulosclerosis and link to hypertensive nephropathy
    Raghu V Durvasula
    Division of Nephrology, University of Washington School of Medicine, Box 356521, Seattle, WA 98195, USA
    Curr Hypertens Rep 8:132-8. 2006
    ..In this review article, we explore the role of a local angiotensin system as a mediator of podocyte injury and discuss its potential link to hypertensive renal disease...
  21. pmc Cyclin-dependent kinase 5 is a regulator of podocyte differentiation, proliferation, and morphology
    Sian V Griffin
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Box 356521, Seattle, WA 98195, USA
    Am J Pathol 165:1175-85. 2004
    ..These data suggest a role for CDK5 as a regulator of podocyte differentiation, proliferation, and morphology...
  22. ncbi request reprint Podocyte injury and targeting therapy: an update
    Raghu V Durvasula
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Box 356521, Seattle, WA 98195, USA
    Curr Opin Nephrol Hypertens 15:1-7. 2006
    ..This review highlights contributions from the past year to our understanding of mechanisms of podocyte injury and implications for potential treatment strategies of glomerular disease...
  23. ncbi request reprint Mechanical strain increases SPARC levels in podocytes: implications for glomerulosclerosis
    Raghu V Durvasula
    Division of Nephrology, Box 356521, Univ of Washington School of Medicine, Seattle, WA 98195, USA
    Am J Physiol Renal Physiol 289:F577-84. 2005
    ..We speculate that the increase in SPARC may be maladaptive and lead to a progressive reduction in podocyte number, thus fueling the future development of glomerulosclerosis...
  24. ncbi request reprint Cell cycle and glomerular disease: a minireview
    Caroline B Marshall
    Division of Nephrology, Department of Medicine, University of Washington, Seattle, WA 98195, USA
    Nephron Exp Nephrol 102:e39-48. 2006
    ..The recent advances in cell cycle biology in diseases of the mesangial cell and the podocyte are the focus of this minireview...
  25. doi request reprint Inducible rodent models of acquired podocyte diseases
    Jeffrey W Pippin
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, 1959 NE Pacific St, Box 356521, Seattle, WA 98195, USA
    Am J Physiol Renal Physiol 296:F213-29. 2009
    ..Details are given on the model backgrounds, how to induce each model, the interpretations of the data, and the benefits and shortcomings of each. Genetic rodent models of podocyte injury are excluded...
  26. doi request reprint Activation of a local renin angiotensin system in podocytes by glucose
    Raghu V Durvasula
    Univ of Washington School of Medicine, Division of Nephrology, Box 356521, Seattle, WA 98195, USA
    Am J Physiol Renal Physiol 294:F830-9. 2008
    ..Taken together, the resultant activation of a local renin angiotensin system by high glucose may promote progressive podocyte injury and loss in diabetic nephropathy...
  27. pmc Role of smooth muscle protein SM22α in glomerular epithelial cell injury
    Caroline B Marshall
    Div of Nephrology, Department of Medicine, Univ of Washington, Seattle, WA 98195, USA
    Am J Physiol Renal Physiol 300:F1026-42. 2011
    ..Furthermore, there was decreased activation of Erk1/2 in diseased SM22α +/+ mice. We conclude that the de novo expression of SM22α in glomerular epithelial cells affects the course of crescentic glomerulonephritis...
  28. ncbi request reprint The cyclin-dependent kinase inhibitor p21 limits murine mesangial proliferative glomerulonephritis
    Toshiaki Monkawa
    Division of Nephrology, University of Washington, Seattle, Washington, USA
    Nephron Exp Nephrol 102:e8-18. 2006
    ..However, the role of p21 in acute mesangial proliferative GN is not known. This study was conducted to test the hypothesis that p21 regulates MC proliferation and apoptosis in anti-MC serum-induced GN...
  29. doi request reprint Creating research infrastructure and functionality to address chronic kidney disease: the Kidney Research Institute
    Jonathan Himmelfarb
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA
    Semin Nephrol 29:457-66. 2009
    ....
  30. doi request reprint The contribution of podocytes to chronic allograft nephropathy
    Jeffrey Pippin
    Nephrology, University of Washington, Seattle, Wash, USA
    Nephron Exp Nephrol 111:e1-10. 2009
    ..The potential role of podocytes in the failing transplanted kidney is unknown. A rat model of kidney transplantation, characterized by proteinuria and glomerulosclerosis, was utilized to examine the potential role of podocytes...
  31. pmc Microarray and bioinformatics analysis of gene expression in experimental membranous nephropathy
    Peter V Hauser
    Division of Nephrology and Hypertension, University of Washington School of Medicine, Seattle, Wash 98195, USA
    Nephron Exp Nephrol 112:e43-58. 2009
    ..Although single genes involved in PHN have been studied, no whole genome-wide expression analysis of kidney tissue has been performed...
  32. ncbi request reprint Induction of TRPC6 channel in acquired forms of proteinuric kidney disease
    Clemens C Möller
    Department of Medicine, Nephrology Division, Massachusetts General Hospital and Harvard Medical School, MGH East, 149 13th Street, Boston, MA 02129, USA
    J Am Soc Nephrol 18:29-36. 2007
    ..These studies suggest the involvement of TRPC6 in the pathology of nongenetic forms of proteinuric disease...
  33. ncbi request reprint Podocyte biology and response to injury
    Peter Mundel
    Division of Nephrology, Albert Einstein College of Medicine, Bronx, New York, USA
    J Am Soc Nephrol 13:3005-15. 2002
  34. pmc De novo expression of podocyte proteins in parietal epithelial cells during experimental glomerular disease
    Takamoto Ohse
    Division of Nephrology, University of Washington, Seattle, Washington 98195 6521, USA
    Am J Physiol Renal Physiol 298:F702-11. 2010
    ..These results are consistent with glomerular cells coexpressing podocyte and PEC proteins in experimental glomerular disease, but not under normal circumstances...
  35. pmc BTBR Ob/Ob mutant mice model progressive diabetic nephropathy
    Kelly L Hudkins
    Department of Pathology, University of Washington, Seattle, Washington, USA
    J Am Soc Nephrol 21:1533-42. 2010
    ..In summary, BTBR ob/ob mice develop a constellation of abnormalities that closely resemble advanced human DN more rapidly than most other murine models, making this strain particularly attractive for testing therapeutic interventions...
  36. doi request reprint p35, the non-cyclin activator of Cdk5, protects podocytes against apoptosis in vitro and in vivo
    Paul T Brinkkoetter
    Division of Nephrology, Department of Medicine, University of Washington, Seattle, Washington 98195 6521, USA
    Kidney Int 77:690-9. 2010
    ..Our study shows that p35 does not affect glomerulogenesis but controls podocyte survival following injury, in part, by regulating Bcl-2 expression...
  37. pmc Retinoic acid inhibits HIV-1-induced podocyte proliferation through the cAMP pathway
    John Cijiang He
    Department of Medicine, Mount Sinai School of Medicine, One Gustave L Levy Place, New York, NY 10029, USA
    J Am Soc Nephrol 18:93-102. 2007
    ..These results demonstrate the mechanism by which atRA reverses the proliferation of podocytes that is induced by HIV-1...
  38. pmc A new function for parietal epithelial cells: a second glomerular barrier
    Takamoto Ohse
    Division of Nephrology, University of Washington, Seattle, WA 98195 6521, USA
    Am J Physiol Renal Physiol 297:F1566-74. 2009
    ..When disturbed following PEC injury, the increase in permeability of this layer to filtered protein is a mechanism underlying periglomerular inflammation characteristic of anti-GBM disease...
  39. ncbi request reprint Cell cycle regulatory proteins in podocyte health and disease
    Caroline B Marshall
    Division of Nephrology, University of Washington, Seattle, WA 98195, USA
    Nephron Exp Nephrol 106:e51-9. 2007
    ..Here, we will review the latest advances in understanding the roles of cell cycle regulatory proteins in diseases of the podocyte...
  40. ncbi request reprint The role of cell cycle proteins in Glomerular disease
    Sian V Griffin
    Department of Medicine, University of Washington, Seattle, WA 98195, USA
    Semin Nephrol 23:569-82. 2003
    ..Defining their roles may lead to potential therapeutic strategies in glomerular disease...
  41. ncbi request reprint Cell cycle control in glomerular disease
    Gunter Wolf
    Department of Medicine, Division of Nephrology, University of Hamburg, Hamburg, Germany
    Prog Cell Cycle Res 5:71-9. 2003
    ..Each leads to glomerular scarring, and a decline in renal function. Studies have shown that these events are critically controlled by cell cycle regulatory proteins, providing potential targets for the development of future therapeutics...
  42. pmc DNA damage is a novel response to sublytic complement C5b-9-induced injury in podocytes
    Jeffrey W Pippin
    Department of Medicine, Division of Nephrology, University of Washington, Seattle, Washington 98195, USA
    J Clin Invest 111:877-85. 2003
    ..These results show that sublytic C5b-9 induces DNA damage in vitro and in vivo and may explain why podocyte proliferation is limited following immune-mediated injury...
  43. ncbi request reprint Cyclin I protects podocytes from apoptosis
    Sian V Griffin
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, 98195, USA
    J Biol Chem 281:28048-57. 2006
    ..Cyclin I protects podocytes from apoptosis, and we provide preliminary data to suggest that this is mediated by stabilization of p21(Cip1/Waf1)...
  44. ncbi request reprint Podocytes that detach in experimental membranous nephropathy are viable
    Arndt T Petermann
    Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Kidney Int 64:1222-31. 2003
    ..Podocyte loss contributes to the development of glomerulosclerosis. Although podocytes have been detected in the urine in certain glomerular diseases, the viability of detached cells is not known...
  45. ncbi request reprint Models of glomerulonephritis
    Raghu V Durvasula
    Division of Nephrology, University of Washington Medical Center, Seattle, WA, USA
    Methods Mol Med 86:47-66. 2003
  46. ncbi request reprint Cell cycle control in glomerular disease
    Sian V Griffin
    Department of Medicine, Division of Nephrology, University of Washington, Box 356521, Seattle, WA 98195, USA
    Springer Semin Immunopathol 24:441-57. 2003
    ..Knowledge of the cell cycle and an understanding of how this may be beneficially manipulated may be crucial to improving the outlook for patients with both diabetic and non-diabetic glomerular disease...
  47. ncbi request reprint Mitotic cell cycle proteins increase in podocytes despite lack of proliferation
    Arndt T Petermann
    Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA
    Kidney Int 63:113-22. 2003
    ..Podocyte proliferation is an uncommon response to glomerular injury and its lack may underlie the development of glomerulosclerosis. However, whether podocytes have the capacity to enter and finish mitosis and cytokinesis is not known...
  48. ncbi request reprint Effects of cyclosporine in osteopontin null mice
    Marilda Mazzali
    Division of Nephrology, Department of Pathology, University of Washington, Seattle, Washington, USA
    Kidney Int 62:78-85. 2002
    ..This study tested the hypothesis that the absence of OPN would ameliorate CsA nephropathy...
  49. ncbi request reprint The cyclin-dependent kinase inhibitor p21 is required for TGF-beta1-induced podocyte apoptosis
    Takehiko Wada
    Division of Nephrology, University of Washington, Seattle, Washington 98195, USA
    Kidney Int 68:1618-29. 2005
    ..The cyclin-dependent kinase (CDK) inhibitor p21 increases in podocytes in diseases where TGF-beta increases. Accordingly, we studied the role of p21 in podocyte apoptosis...
  50. pmc Rosuvastatin protects against podocyte apoptosis in vitro
    Fionnuala C Cormack-Aboud
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Seattle, WA98195, USA
    Nephrol Dial Transplant 24:404-12. 2009
    ..Therefore, we queried whether rosuvastatin is prosurvival in podocytes through a p21-dependent pathway...
  51. pmc Establishment of conditionally immortalized mouse glomerular parietal epithelial cells in culture
    Takamoto Ohse
    Department of Medicine, Division of Nephrology, University of Washington, Seattle, WA 98195 6521, USA
    J Am Soc Nephrol 19:1879-90. 2008
    ..This mPEC line will assist in future mechanistic studies of PEC and enhance our understanding of glomerular injury...
  52. doi request reprint Dexamethasone's prosurvival benefits in podocytes require extracellular signal-regulated kinase phosphorylation
    Takehiko Wada
    Division of Nephrology, University of Washington, Seattle, WA 98195, USA
    Nephron Exp Nephrol 109:e8-19. 2008
    ..However, the precise mechanisms underlying the beneficial effects of glucocorticoids on podocytes remain to be fully elucidated...
  53. pmc Protease nexin-1, tPA, and PAI-1 are upregulated in cryoglobulinemic membranoproliferative glomerulonephritis
    Sekiko Taneda
    Department of Pathology, Division of Nephrology, University of Washington, Seattle, Washington 98195, USA
    J Am Soc Nephrol 19:243-51. 2008
  54. ncbi request reprint Insulin is a potent survival factor in mesangial cells: role of the PI3-kinase/Akt pathway
    Keiju Hiromura
    Division of Nephrology, Department of Medicine, University of Washington School of Medicine, Seattle, Washington, USA
    Kidney Int 61:1312-21. 2002
    ..However, little is known about the anti-apoptotic effect of insulin and the role of the PI3-kinase/Akt pathway in mesangial cells (MC) apoptosis...
  55. ncbi request reprint Familial nephrotic syndrome: PLCE1 enters the fray
    Jonathan Ashley Jefferson
    Division of Nephrology, University of Washington, 1959 NE Pacific Street, Box 356521, Seattle, Washington 98195, USA
    Nephrol Dial Transplant 22:1849-52. 2007
  56. ncbi request reprint Viable podocytes detach in experimental diabetic nephropathy: potential mechanism underlying glomerulosclerosis
    Arndt T Petermann
    Department of Medicine, Division of Nephrology, University of Washington School of Medicine, Seattle, Wash 98195, USA
    Nephron Exp Nephrol 98:e114-23. 2004
    ..A decrease in podocyte number contributes to the development of glomerulosclerosis in diabetic nephropathy. Although podocytes have been detected in the urine in certain glomerular diseases, their viability is poorly understood...
  57. pmc Therapeutics in renal disease: the road ahead for antiproliferative targets
    Peter J Nelson
    Division of Nephrology, New York University School of Medicine, New York, NY 10016, USA
    Nephron Exp Nephrol 103:e6-15. 2006
    ..Systems research to clarify these issues should accelerate the development of this promising therapeutic strategy...
  58. ncbi request reprint The hypertrophic effect of transforming growth factor-beta is reduced in the absence of cyclin-dependent kinase-inhibitors p21 and p27
    Toshiaki Monkawa
    Department of Medicine, Division of Nephrology, University of Washington, Seattle, Washington 98195, USA
    J Am Soc Nephrol 13:1172-8. 2002
    ..However, the hypertrophic growth effects of TGF-beta are reduced in the absence of both p21 and p27. These data suggest that the regulation of the antiproliferative and hypertrophic effects of TGF-beta may be distinct processes...
  59. ncbi request reprint p27(Kip1) Knockout mice are protected from diabetic nephropathy: evidence for p27(Kip1) haplotype insufficiency
    Gunter Wolf
    Klinik fur Innere Medizin III, University of Jena, Jena, Germany
    Kidney Int 68:1583-9. 2005
    ..However, it is unclear whether deletion of p27(Kip1) protects the kidneys of diabetic nephropathy in vivo...
  60. ncbi request reprint P27Kip1: the "rosebud" of diabetic nephropathy?
    Gunter Wolf
    J Am Soc Nephrol 14:819-22. 2003
  61. ncbi request reprint Cyclooxygenase-2 overexpression inhibits platelet-derived growth factor-induced mesangial cell proliferation through induction of the tumor suppressor gene p53 and the cyclin-dependent kinase inhibitors p21waf-1/cip-1 and p27kip-1
    Gunther Zahner
    Department of Medicine, Division of Nephrology and Osteology, University of Hamburg, 20246 Hamburg, Germany
    J Biol Chem 277:9763-71. 2002
    ..These data suggest that COX-2 inhibits mesangial cell proliferation by a novel mechanism that is independent of prostaglandin synthesis, but involves p53, p21(cip-1), and p27(kip-1)...
  62. pmc Differential expression of d-type cyclins in podocytes in vitro and in vivo
    Arndt Petermann
    Universitätsklinikum RWTH Aachen, Aachen, Germany
    Am J Pathol 164:1417-24. 2004
    ..Cyclin D1 is not necessary for the terminal differentiation of podocytes, and expression coincides with cell-cycle entry. In contrast, cyclin D3 expression coincides with podocyte differentiation and quiescence...
  63. ncbi request reprint Urinary podocyte loss is a more specific marker of ongoing glomerular damage than proteinuria
    Donghai Yu
    Department of Medicine, Division of Nephrology and Clinical Immunology, University of Aachen, Germany
    J Am Soc Nephrol 16:1733-41. 2005
    ..The data suggest that podocyturia may become a more sensitive means to assess the activity of glomerular damage than proteinuria...
  64. ncbi request reprint Angiotensin II-induced hypertrophy of proximal tubular cells requires p27Kip1
    Gunter Wolf
    Division of Nephrology and Osteology, Department of Medicine, University of Hamburg, Hamburg, Germany
    Kidney Int 64:71-81. 2003
    ....
  65. ncbi request reprint Negatively regulating the cell cycle can be positive
    Keiju Hiromura
    J Am Soc Nephrol 15:1361-2. 2004
  66. ncbi request reprint The rapamycin derivative RAD inhibits mesangial cell migration through the CDK-inhibitor p27KIP1
    Christoph Daniel
    Medizinische Klinik IV, Universitat Erlangen Nurnberg, Erlangen, Germany
    Lab Invest 84:588-96. 2004
    ..Moreover, RAD-induced inhibition of MC migration in vitro is partially mediated by the CDK-inhibitor p27(KIP1), but not p21(CIP1)...
  67. ncbi request reprint Not just an inhibitor: a role for p21 beyond the cell cycle-"The truth is rarely pure and never simple"
    Sian V Griffin
    J Am Soc Nephrol 15:825-6. 2004
  68. ncbi request reprint Hematopoietic stem cells contribute to the regeneration of renal tubules after renal ischemia-reperfusion injury in mice
    Fangming Lin
    Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Mail Code 9063, Dallas, TX 75390 9063, USA
    J Am Soc Nephrol 14:1188-99. 2003
    ..This is the first report to show that HSC can differentiate into renal tubular cells after I/R injury. Because of their availability, HSC may be useful for cell replacement therapy of acute renal failure...
  69. ncbi request reprint Cellular response to injury in membranous nephropathy
    Masaomi Nangaku
    Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, Tokyo, Japan
    J Am Soc Nephrol 16:1195-204. 2005
    ..Improved understanding of the role of complement in the pathogenesis of MN and of the cellular response to C5b-9 attack creates several new opportunities for therapeutic intervention that may benefit patients with MN in the future...
  70. ncbi request reprint Glial cell line-derived neurotrophic factor and its receptor ret is a novel ligand-receptor complex critical for survival response during podocyte injury
    Cynthia C Tsui
    Department of Biological Sciences, University at Buffalo The State University of New York, 109 Cooke Hall, North Campus, Buffalo, NY 14260, USA
    J Am Soc Nephrol 17:1543-52. 2006
    ..Furthermore, Ret is highly upregulated during podocyte injury in vitro and in vivo, suggesting that Ret activation is a critical adaptive response for podocyte remodeling and repair...

Research Grants26

  1. Cell Cycle and Podocyte Apoptosis
    Stuart Shankland; Fiscal Year: 2009
    ..The overall goal is to delineate new paradigms in the regulation of podocyte survival and death, so that ultimately new strategies can be developed to prevent podocyte loss, enhance kidney survival, and reduce kidney disease. ..
  2. Cell Cycle and Podocyte Apoptosis
    Stuart Shankland; Fiscal Year: 2007
    ..The overall goal is to delineate new paradigms in the regulation of podocyte survival and death, so that ultimately new strategies can be developed to prevent podocyte loss, enhance kidney survival, and reduce kidney disease. ..
  3. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2003
    ..Our ultimate goal is to show novel roles for specific cell cycle proteins in glomerular disease, so that specific therapeutic strategies can be developed to reduce glomerular injury. ..
  4. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2002
    ..Our ultimate goal is to show novel roles for specific cell cycle proteins in glomerular disease, so that specific therapeutic strategies can be developed to reduce glomerular injury. ..
  5. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2001
    ..Our ultimate goal is to show novel roles for specific cell cycle proteins in glomerular disease, so that specific therapeutic strategies can be developed to reduce glomerular injury. ..
  6. CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSIS
    Stuart Shankland; Fiscal Year: 2000
    ..Our ultimate goal is to show novel roles for specific cell cycle proteins in glomerular disease, so that specific therapeutic strategies can be developed to reduce glomerular injury. ..
  7. Cell Cycle and Podocyte Apoptosis
    Stuart Shankland; Fiscal Year: 2009
    ..The overall goal is to delineate new paradigms in the regulation of podocyte survival and death, so that ultimately new strategies can be developed to prevent podocyte loss, enhance kidney survival, and reduce kidney disease. ..
  8. 6th International Podocyte Conference
    Stuart Shankland; Fiscal Year: 2006
    ..Moreover, this is an exciting era in podocytes biology given the large body of literature that has been published in the past 2-5 years. ..
  9. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2005
    ..The ultimate goal is to identify new targets for potential therapies in order to reduce the heavy burden of disease in patients with gIomerular disease. ..
  10. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2007
    ..The ultimate goal is to identify new targets for potential therapies in order to reduce the heavy burden of disease in patients with gIomerular disease. ..
  11. RESEARCH TRAINING IN RENAL DISEASE
    Stuart Shankland; Fiscal Year: 2007
    ..William Couser who has been the Program Director for the past 19 years. It will be co-directed by Dr. Stuart Shankland, an active basic investigator in nephrology. Seven physicians in nephrology will serve as primary mentors...
  12. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2006
    ..The ultimate goal is to identify new targets for potential therapies in order to reduce the heavy burden of disease in patients with gIomerular disease. ..
  13. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2005
    ..The ultimate goal is to identify new targets for potential therapies in order to reduce the heavy burden of disease in patients with gIomerular disease. ..
  14. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 1999
    ..Insights into the mechanisms of mesangial cell proliferation may provide future therapeutic strategies for glomerular disease. ..
  15. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2000
    ..Insights into the mechanisms of mesangial cell proliferation may provide future therapeutic strategies for glomerular disease. ..
  16. MECHANISMS OF PODOCYTE INJURY
    Stuart Shankland; Fiscal Year: 2002
    ..Taken together, the overall goal is to show novel mechanisms underlying podo injury, so that ultimately, specific therapeutic strategies can be developed to reduce podo injury in the development of glomerular sclerosis. ..
  17. MECHANISMS OF PODOCYTE INJURY
    Stuart Shankland; Fiscal Year: 2003
    ..Taken together, the overall goal is to show novel mechanisms underlying podo injury, so that ultimately, specific therapeutic strategies can be developed to reduce podo injury in the development of glomerular sclerosis. ..
  18. MECHANISMS OF PODOCYTE INJURY
    Stuart Shankland; Fiscal Year: 2004
    ..Taken together, the overall goal is to show novel mechanisms underlying podo injury, so that ultimately, specific therapeutic strategies can be developed to reduce podo injury in the development of glomerular sclerosis. ..
  19. CELL CYCLE CONTROL IN GLOMERULAR DISEASE
    Stuart Shankland; Fiscal Year: 2004
    ..The ultimate goal is to identify new targets for potential therapies in order to reduce the heavy burden of disease in patients with gIomerular disease. ..
  20. 5TH INTERNATIONAL PODOCYTE CONFERENCE
    Stuart Shankland; Fiscal Year: 2004
    ..3. To facilitate cross-talk between clinicians and scientists with the ultimate goal of improving prognosis, treatment and care of patients with glomerular disease. ..
  21. MECHANISMS OF PODOCYTE INJURY
    Stuart Shankland; Fiscal Year: 2005
    ..Taken together, the overall goal is to show novel mechanisms underlying podo injury, so that ultimately, specific therapeutic strategies can be developed to reduce podo injury in the development of glomerular sclerosis. ..