Literature DB >> 19755471

Expression of sialidase and dystroglycan in human glomerular diseases.

Nils P J Vogtländer1, Johan van der Vlag, Marinka A H Bakker, Henry B Dijkman, Ron A Wevers, Kevin P Campbell, Jack F M Wetzels, Jo H M Berden.   

Abstract

BACKGROUND: alpha-Dystroglycan (alpha-DG) is a negatively charged glycoprotein that covers the surface of podocytes. A decreased glomerular expression of alpha-DG has been described in minimal change nephropathy (MCN), but not in focal segmental glomerulosclerosis (FSGS). This was suggested as a tool to distinguish these diseases. Sialic acid is a negatively charged carbohydrate extensively present on both alpha-DG and podocalyxin, which is also expressed on podocytes. Intrarenal perfusion with bacterial sialidase leads to foot process effacement and proteinuria. This is the first study on the expression of endogenous glomerular sialidase; furthermore, the expression of dystroglycan was re-evaluated.
METHODS: The expression of alpha-DG and sialidase was investigated by immunofluorescence in kidney biopsies of patients with MCN (n = 5), FSGS (n = 15), proliferative lupus nephritis (LN, n = 9), membranous glomerulopathy (MG, n = 10) and normal human kidneys (NHK, n = 4). The urinary sialic acid concentration was measured using a newly developed LC-tandem mass spectrometry method.
RESULTS: A 3-fold increased glomerular expression of sialidase was found in MG, accompanied with an increased urinary sialic acid concentration in two MG patients. However, we did not observe major changes in the expression of alpha-DG in patients with the above-mentioned glomerular diseases compared to NHK, also not between MCN and FSGS.
CONCLUSIONS: Endogenous glomerular sialidase expression is increased in MG, which might represent a novel mechanism for the loss of negative charge in the glomerular capillary filter. The expression of dystroglycan cannot be used as a diagnostic tool to differentiate between glomerular diseases.

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Year:  2009        PMID: 19755471     DOI: 10.1093/ndt/gfp465

Source DB:  PubMed          Journal:  Nephrol Dial Transplant        ISSN: 0931-0509            Impact factor:   5.992


  9 in total

Review 1.  Pathogenesis of proteinuria in idiopathic minimal change disease: molecular mechanisms.

Authors:  Gabriel Cara-Fuentes; William L Clapp; Richard J Johnson; Eduardo H Garin
Journal:  Pediatr Nephrol       Date:  2016-07-06       Impact factor: 3.714

Review 2.  Minimal change disease and idiopathic FSGS: manifestations of the same disease.

Authors:  Rutger J Maas; Jeroen K Deegens; Bart Smeets; Marcus J Moeller; Jack F Wetzels
Journal:  Nat Rev Nephrol       Date:  2016-10-17       Impact factor: 28.314

3.  Podocyte-Specific Sialylation-Deficient Mice Serve as a Model for Human FSGS.

Authors:  Kristina M Niculovic; Linda Blume; Henri Wedekind; Elina Kats; Iris Albers; Stephanie Groos; Markus Abeln; Jessica Schmitz; Esther Beuke; Jan H Bräsen; Anette Melk; Mario Schiffer; Birgit Weinhold; Anja K Münster-Kühnel
Journal:  J Am Soc Nephrol       Date:  2019-04-30       Impact factor: 10.121

Review 4.  The role of cell-extracellular matrix interactions in glomerular injury.

Authors:  Corina M Borza; Ambra Pozzi
Journal:  Exp Cell Res       Date:  2012-03-05       Impact factor: 3.905

5.  The Gne M712T mouse as a model for human glomerulopathy.

Authors:  Sravan Kakani; Tal Yardeni; Justin Poling; Carla Ciccone; Terren Niethamer; Enriko D Klootwijk; Irini Manoli; Daniel Darvish; Shelley Hoogstraten-Miller; Patricia Zerfas; E Tian; Kelly G Ten Hagen; Jeffrey B Kopp; William A Gahl; Marjan Huizing
Journal:  Am J Pathol       Date:  2012-02-07       Impact factor: 4.307

6.  Detection of activated parietal epithelial cells on the glomerular tuft distinguishes early focal segmental glomerulosclerosis from minimal change disease.

Authors:  Bart Smeets; Fabien Stucker; Jack Wetzels; Isabelle Brocheriou; Pierre Ronco; Hermann-Josef Gröne; Vivette D'Agati; Agnes B Fogo; Toin H van Kuppevelt; Hans-Peter Fischer; Peter Boor; Jürgen Floege; Tammo Ostendorf; Marcus J Moeller
Journal:  Am J Pathol       Date:  2014-10-07       Impact factor: 4.307

7.  Accumulation of long-chain glycosphingolipids during aging is prevented by caloric restriction.

Authors:  María José Hernández-Corbacho; Russell W Jenkins; Christopher J Clarke; Yusuf A Hannun; Lina M Obeid; Ashley J Snider; Leah J Siskind
Journal:  PLoS One       Date:  2011-06-08       Impact factor: 3.240

8.  Glycoprotein hyposialylation gives rise to a nephrotic-like syndrome that is prevented by sialic acid administration in GNE V572L point-mutant mice.

Authors:  Mitutoshi Ito; Kazushi Sugihara; Tomoya Asaka; Tadashi Toyama; Toru Yoshihara; Kengo Furuichi; Takashi Wada; Masahide Asano
Journal:  PLoS One       Date:  2012-01-13       Impact factor: 3.240

9.  Podocin and beta dystroglycan expression to study podocyte-podocyte and basement membrane matrix connections in adult protienuric states.

Authors:  Praveen B Shankar; Ritambhra Nada; Kusum Joshi; Ashwani Kumar; Charan Singh Rayat; Vinay Sakhuja
Journal:  Diagn Pathol       Date:  2014-02-21       Impact factor: 2.644

  9 in total

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