2009
DOI: 10.1152/ajprenal.90421.2008
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Abstract: Pippin JW, Brinkkoetter PT, Cormack-Aboud FC, Durvasula RV, Hauser PV, Kowalewska J, Krofft RD, Logar CM, Marshall CB, Ohse T, Shankland SJ. Inducible rodent models of acquired podocyte diseases. Am J Physiol Renal Physiol 296: F213-F229, 2009. First published September 10, 2008 doi:10.1152/ajprenal.90421.2008.-Glomerular diseases remain the leading cause of chronic and end-stage kidney disease. Significant advances in our understanding of human glomerular diseases have been enabled by the development and bet… Show more

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Cited by 231 publications
(259 citation statements)
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“…27 As shown in Figure 1A, immunofluorescence staining showed that WT1-positive cells were dramatically reduced in a time-dependent manner after ADR injection. Quantitative determination of the WT1-positive podocytes in mouse kidneys at 1, 3, and 5 weeks after ADR injection is presented in Figure 1B.…”
Section: Loss Of Wt1 In Adriamycin Nephropathy Is Not Caused By Podocmentioning
confidence: 75%
“…27 As shown in Figure 1A, immunofluorescence staining showed that WT1-positive cells were dramatically reduced in a time-dependent manner after ADR injection. Quantitative determination of the WT1-positive podocytes in mouse kidneys at 1, 3, and 5 weeks after ADR injection is presented in Figure 1B.…”
Section: Loss Of Wt1 In Adriamycin Nephropathy Is Not Caused By Podocmentioning
confidence: 75%
“…Magnetic-bead isolation of capsulated and decapsulated glomeruli from wild-type mice following differential size sieving of digested kidneys was performed as described previously, 23 with isolated glomeruli immediately lysed in RIPA buffer (Teknova, Hollister, CA, USA) containing Complete Protease Inhibitor (Roche, Indianapolis, IN, USA), 50 mM sodium fluoride and 0.1 mM sodium orthovanadate at 41C to collect total protein. Passive NTN 24 was induced in cohorts of male SSeCKS þ / þ mice (n ¼ 5) and male SSeCKS À/À mice (n ¼ 5) at 15 weeks of age by intraperitoneal injection of nephrotoxic immunoglobulin (12.5 mg/20 g body weight), or an equivalent volume of vehicle (1 Â PBS, pH 7.4), on 2 consecutive days. Urine was collected from each mouse on day 14 after the second intraperitoneal injection immediately before collection, formalin fixation and paraffin embedding of kidneys.…”
Section: Materials and Methods Micementioning
confidence: 99%
“…[3][4][5] We therefore studied the expression of SSeCKS in archival tissue from models with existing glomerular disease representing a spectrum of podocytopathies, 30 specifically the following: Tg26 (a model of collapsing glomerulopathy), 20 mice with passive NTN (a model of crescentic glomerulonephritis), 24 rats with PAN (a model of minimal change disease), 24 rats with PHN (a model of membranous nephropathy), 24 and mice with AN (a model of focal segmental glomerulosclerosis). 24 Examination of these diseased models suggests that SSeCKSpositive PECs are major constituents of extracapillary glomerular lesions. In the proliferative podocytopathies of Tg26 and NTN, SSeCKS was expressed throughout the crescentic lesions of these models (Figure 5b and c).…”
Section: Expression Of Ssecks In Models Of Podocytopathiesmentioning
confidence: 99%
“…We first used the protamine sulfate model, where perfusion of protamine sulfate causes rapid foot process effacement, which can be reversed through subsequent perfusion with heparin sulfate. 8,31 Kidneys within nephrin WT/WT and nephrin Y3F/Y3F mice were perfused with HBSS control buffer, protamine sulfate, or protamine sulfate followed by heparin sulfate, fixed, and analyzed by EM. Compared with buffer-treated animals, mice from both genotypes perfused with protamine sulfate showed extensive foot process spreading ( Figure 6, A and B).…”
Section: C57bl/6 Nephrinmentioning
confidence: 99%