Administration of Recombinant Soluble Urokinase Receptor Per Se Is Not Sufficient to Induce Podocyte Alterations and Proteinuria in Mice

Dominique Cathelin; Sandrine Placier; Michael Ploug; Marie-Christine Verpont; Sophie Vandermeersch; Yosu Luque; Alexandre Hertig; Eric Rondeau; Laurent Mesnard

doi:10.1681/asn.2013040425

Administration of Recombinant Soluble Urokinase Receptor Per Se Is Not Sufficient to Induce Podocyte Alterations and Proteinuria in Mice

Dominique Cathelin, Sandrine Placier, Michael Ploug, Marie-Christine Verpont, Sophie Vandermeersch, Yosu Luque, Alexandre Hertig, Eric Rondeau, Laurent Mesnard

54 Citations (Scopus)

Abstract

Circulating levels of soluble forms of urokinase-type plasminogen activator receptor (suPAR) are generally elevated in sera from children and adults with FSGS compared with levels in healthy persons or those with other types of kidney disease. In mice lacking the gene encoding uPAR, forced increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria. However, whether overexpression of suPAR, per se, contributes to the pathogenesis of FSGS in humans remains controversial. We conducted an independent set of animal experiments in which two different and well characterized forms of recombinant suPAR produced by eukaryotic cells were administered over the short or long term to wild-type (WT) mice. In accordance with the previous study, the delivered suPARs are deposited in the glomeruli. However, such deposition of either form of suPAR in the kidney did not result in increased glomerular proteinuria or altered podocyte architecture. Our findings suggest that glomerular deposits of suPAR caused by elevated plasma levels are not sufficient to engender albuminuria.

Original language	English
Journal	Journal of the American Society of Nephrology
Volume	25
Issue number	8
Pages (from-to)	1662-1668
Number of pages	7
ISSN	1046-6673
DOIs	https://doi.org/10.1681/asn.2013040425
Publication status	Published - 1 Aug 2014

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Cathelin, D., Placier, S., Ploug, M., Verpont, M-C., Vandermeersch, S., Luque, Y., Hertig, A., Rondeau, E., & Mesnard, L. (2014). Administration of Recombinant Soluble Urokinase Receptor Per Se Is Not Sufficient to Induce Podocyte Alterations and Proteinuria in Mice. Journal of the American Society of Nephrology, 25(8), 1662-1668. https://doi.org/10.1681/asn.2013040425

Administration of Recombinant Soluble Urokinase Receptor Per Se Is Not Sufficient to Induce Podocyte Alterations and Proteinuria in Mice. / Cathelin, Dominique; Placier, Sandrine; Ploug, Michael et al.

In: Journal of the American Society of Nephrology, Vol. 25, No. 8, 01.08.2014, p. 1662-1668.

Research output: Contribution to journal › Journal article › Research › peer-review

Cathelin, D, Placier, S, Ploug, M, Verpont, M-C, Vandermeersch, S, Luque, Y, Hertig, A, Rondeau, E & Mesnard, L 2014, 'Administration of Recombinant Soluble Urokinase Receptor Per Se Is Not Sufficient to Induce Podocyte Alterations and Proteinuria in Mice', Journal of the American Society of Nephrology, vol. 25, no. 8, pp. 1662-1668. https://doi.org/10.1681/asn.2013040425

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title = "Administration of Recombinant Soluble Urokinase Receptor Per Se Is Not Sufficient to Induce Podocyte Alterations and Proteinuria in Mice",

abstract = "Circulating levels of soluble forms of urokinase-type plasminogen activator receptor (suPAR) are generally elevated in sera from children and adults with FSGS compared with levels in healthy persons or those with other types of kidney disease. In mice lacking the gene encoding uPAR, forced increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria. However, whether overexpression of suPAR, per se, contributes to the pathogenesis of FSGS in humans remains controversial. We conducted an independent set of animal experiments in which two different and well characterized forms of recombinant suPAR produced by eukaryotic cells were administered over the short or long term to wild-type (WT) mice. In accordance with the previous study, the delivered suPARs are deposited in the glomeruli. However, such deposition of either form of suPAR in the kidney did not result in increased glomerular proteinuria or altered podocyte architecture. Our findings suggest that glomerular deposits of suPAR caused by elevated plasma levels are not sufficient to engender albuminuria.",

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AU - Cathelin, Dominique

AU - Placier, Sandrine

AU - Ploug, Michael

AU - Verpont, Marie-Christine

AU - Vandermeersch, Sophie

AU - Luque, Yosu

AU - Hertig, Alexandre

AU - Rondeau, Eric

AU - Mesnard, Laurent

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N2 - Circulating levels of soluble forms of urokinase-type plasminogen activator receptor (suPAR) are generally elevated in sera from children and adults with FSGS compared with levels in healthy persons or those with other types of kidney disease. In mice lacking the gene encoding uPAR, forced increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria. However, whether overexpression of suPAR, per se, contributes to the pathogenesis of FSGS in humans remains controversial. We conducted an independent set of animal experiments in which two different and well characterized forms of recombinant suPAR produced by eukaryotic cells were administered over the short or long term to wild-type (WT) mice. In accordance with the previous study, the delivered suPARs are deposited in the glomeruli. However, such deposition of either form of suPAR in the kidney did not result in increased glomerular proteinuria or altered podocyte architecture. Our findings suggest that glomerular deposits of suPAR caused by elevated plasma levels are not sufficient to engender albuminuria.

AB - Circulating levels of soluble forms of urokinase-type plasminogen activator receptor (suPAR) are generally elevated in sera from children and adults with FSGS compared with levels in healthy persons or those with other types of kidney disease. In mice lacking the gene encoding uPAR, forced increases in suPAR concentration result in FSGS-like glomerular lesions and proteinuria. However, whether overexpression of suPAR, per se, contributes to the pathogenesis of FSGS in humans remains controversial. We conducted an independent set of animal experiments in which two different and well characterized forms of recombinant suPAR produced by eukaryotic cells were administered over the short or long term to wild-type (WT) mice. In accordance with the previous study, the delivered suPARs are deposited in the glomeruli. However, such deposition of either form of suPAR in the kidney did not result in increased glomerular proteinuria or altered podocyte architecture. Our findings suggest that glomerular deposits of suPAR caused by elevated plasma levels are not sufficient to engender albuminuria.

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Administration of Recombinant Soluble Urokinase Receptor Per Se Is Not Sufficient to Induce Podocyte Alterations and Proteinuria in Mice

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