Experts and Doctors on podocytes in Ottawa, Ontario, Canada

Summary

Locale: Ottawa, Ontario, Canada
Topic: podocytes

Top Publications

  1. Michaud J, Chaisson K, Parks R, Kennedy C. FSGS-associated alpha-actinin-4 (K256E) impairs cytoskeletal dynamics in podocytes. Kidney Int. 2006;70:1054-61 pubmed
    ..Such intrinsic cytoskeletal derangements may underlie initial podocyte damage and foot process effacement encountered in ACTN4-associated FSGS. ..
  2. Michaud J, Stitt Cavanaugh E, Endlich N, Endlich K, De Repentigny Y, Kothary R, et al. Mice with podocyte-specific overexpression of wild type alpha-actinin-4 are healthy controls for K256E-alpha-actinin-4 mutant transgenic mice. Transgenic Res. 2010;19:285-9 pubmed publisher
    ..These findings suggest that the K256E mutation itself and not overexpression of alpha-actinin-4 protein per se accounts for the FSGS phenotype in our transgenic model. ..
  3. Stitt Cavanagh E, Faour W, Takami K, Carter A, Vanderhyden B, Guan Y, et al. A maladaptive role for EP4 receptors in podocytes. J Am Soc Nephrol. 2010;21:1678-90 pubmed publisher
    ..05). These findings suggest that prostaglandin E(2), acting via EP4 receptors contributes to podocyte injury and compromises the glomerular filtration barrier. ..
  4. Nadarajah R, Milagres R, Dilauro M, Gutsol A, Xiao F, Zimpelmann J, et al. Podocyte-specific overexpression of human angiotensin-converting enzyme 2 attenuates diabetic nephropathy in mice. Kidney Int. 2012;82:292-303 pubmed publisher
    ..Thus, the podocyte-specific overexpression of human ACE2 transiently attenuates the development of diabetic nephropathy. ..
  5. Read N, Gutsol A, Holterman C, Carter A, Coulombe J, Gray D, et al. Ubiquitin C-terminal hydrolase L1 deletion ameliorates glomerular injury in mice with ACTN4-associated focal segmental glomerulosclerosis. Biochim Biophys Acta. 2014;1842:1028-40 pubmed publisher

Detail Information

Publications5

  1. Michaud J, Chaisson K, Parks R, Kennedy C. FSGS-associated alpha-actinin-4 (K256E) impairs cytoskeletal dynamics in podocytes. Kidney Int. 2006;70:1054-61 pubmed
    ..Such intrinsic cytoskeletal derangements may underlie initial podocyte damage and foot process effacement encountered in ACTN4-associated FSGS. ..
  2. Michaud J, Stitt Cavanaugh E, Endlich N, Endlich K, De Repentigny Y, Kothary R, et al. Mice with podocyte-specific overexpression of wild type alpha-actinin-4 are healthy controls for K256E-alpha-actinin-4 mutant transgenic mice. Transgenic Res. 2010;19:285-9 pubmed publisher
    ..These findings suggest that the K256E mutation itself and not overexpression of alpha-actinin-4 protein per se accounts for the FSGS phenotype in our transgenic model. ..
  3. Stitt Cavanagh E, Faour W, Takami K, Carter A, Vanderhyden B, Guan Y, et al. A maladaptive role for EP4 receptors in podocytes. J Am Soc Nephrol. 2010;21:1678-90 pubmed publisher
    ..05). These findings suggest that prostaglandin E(2), acting via EP4 receptors contributes to podocyte injury and compromises the glomerular filtration barrier. ..
  4. Nadarajah R, Milagres R, Dilauro M, Gutsol A, Xiao F, Zimpelmann J, et al. Podocyte-specific overexpression of human angiotensin-converting enzyme 2 attenuates diabetic nephropathy in mice. Kidney Int. 2012;82:292-303 pubmed publisher
    ..Thus, the podocyte-specific overexpression of human ACE2 transiently attenuates the development of diabetic nephropathy. ..
  5. Read N, Gutsol A, Holterman C, Carter A, Coulombe J, Gray D, et al. Ubiquitin C-terminal hydrolase L1 deletion ameliorates glomerular injury in mice with ACTN4-associated focal segmental glomerulosclerosis. Biochim Biophys Acta. 2014;1842:1028-40 pubmed publisher