Literature DB >> 15149332

Selective impairment of gene expression and assembly of nephrin in human diabetic nephropathy.

Ariela Benigni1, Elena Gagliardini, Susanna Tomasoni, Mauro Abbate, Piero Ruggenenti, Raghu Kalluri, Giuseppe Remuzzi.   

Abstract

BACKGROUND: Recent disclosure of podocyte proteins has unraveled previously rather mysterious mechanisms that govern glomerular perm-selectivity in health and disease. Here we addressed the role of nephrin, CD2-associated protein (CD2AP), and podocin together with the integrity of the slit diaphragm in the pathogenesis of proteinuria of patients with diabetes and nephropathy.
METHODS: Nephrin mRNA and protein expression were evaluated in parallel in adult diabetic patients by in situ hybridization and immunohistochemistry. For comparison, nondiabetic patients with minimal change nephrosis and normal control patients were evaluated. CD2AP and podocin expression by immunohistochemistry was also assessed. The filtration slit was analyzed by morphometry and transmission electron microscopy.
RESULTS: Extracellular nephrin mRNA and protein were markedly reduced in diabetic patients. No changes were found in patients with minimal change versus controls. CD2AP and podocin were comparable in all subjects. Ultrastructural analysis showed in diabetic patients a remarkable reduction in the percentage of electron dense slit diaphragms, despite a frequency of the filtration slits comparable to control patients.
CONCLUSION: Down-regulation of nephrin and loss of the electron dense structure of slit diaphragm indicate a novel mechanism accounting for proteinuria in diabetic nephropathy. To the extent that glomerular protein trafficking contributes to renal disease progression, our findings may have clinical relevance. Reduction of nephrin in the context of normal expression of CD2AP and podocin can be taken reasonably as a specific marker of renal disease in diabetes. Therapies targeted at correcting podocyte nephrin might be of value for diabetic medicine.

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Year:  2004        PMID: 15149332     DOI: 10.1111/j.1523-1755.2004.00636.x

Source DB:  PubMed          Journal:  Kidney Int        ISSN: 0085-2538            Impact factor:   10.612


  38 in total

1.  Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease.

Authors:  Akihiro Fukuda; Larysa T Wickman; Madhusudan P Venkatareddy; Yuji Sato; Mahboob A Chowdhury; Su Q Wang; Kerby A Shedden; Robert C Dysko; Jocelyn E Wiggins; Roger C Wiggins
Journal:  Kidney Int       Date:  2011-09-21       Impact factor: 10.612

Review 2.  Antiproteinuric effect of RAS blockade: new mechanisms.

Authors:  Markus Lassila; Mark E Cooper; Karin Jandeleit-Dahm
Journal:  Curr Hypertens Rep       Date:  2004-10       Impact factor: 5.369

3.  Imaging of the porous ultrastructure of the glomerular epithelial filtration slit.

Authors:  Elena Gagliardini; Sara Conti; Ariela Benigni; Giuseppe Remuzzi; Andrea Remuzzi
Journal:  J Am Soc Nephrol       Date:  2010-10-28       Impact factor: 10.121

4.  Protective effects of low-dose rapamycin combined with valsartan on podocytes of diabetic rats.

Authors:  Jin Zhang; Xiaozhou Hu; Shaoting Wang; Yan Zhang; Hong Yang
Journal:  Int J Clin Exp Med       Date:  2015-08-15

5.  Activation of adenosine 2A receptors preserves structure and function of podocytes.

Authors:  Alaa S Awad; Michael Rouse; Lixia Liu; Amy L Vergis; Diane L Rosin; Joel Linden; John R Sedor; Mark D Okusa
Journal:  J Am Soc Nephrol       Date:  2007-11-28       Impact factor: 10.121

6.  C3a receptor blockade protects podocytes from injury in diabetic nephropathy.

Authors:  Marina Morigi; Luca Perico; Daniela Corna; Monica Locatelli; Paola Cassis; Claudia Elisa Carminati; Silvia Bolognini; Carlamaria Zoja; Giuseppe Remuzzi; Ariela Benigni; Simona Buelli
Journal:  JCI Insight       Date:  2020-03-12

Review 7.  Regenerative medicine in kidney disease: where we stand and where to go.

Authors:  Fernanda T Borges; Nestor Schor
Journal:  Pediatr Nephrol       Date:  2017-07-22       Impact factor: 3.714

8.  The human nephrin Y1139RSL motif is essential for podocyte foot process organization and slit diaphragm formation during glomerular development.

Authors:  Eugenel B Espiritu; Huajun Jiang; Sophie Moreau-Marquis; Mara Sullivan; Kunimasa Yan; Donna Beer Stolz; Matthew G Sampson; Neil A Hukriede; Agnieszka Swiatecka-Urban
Journal:  J Biol Chem       Date:  2019-05-31       Impact factor: 5.157

9.  Mineralocorticoid receptor blockade enhances the antiproteinuric effect of an angiotensin II blocker through inhibiting podocyte injury in type 2 diabetic rats.

Authors:  Akira Nishiyama; Hiroyuki Kobori; Yoshio Konishi; Takashi Morikawa; Isseki Maeda; Michiaki Okumura; Masatsugu Kishida; Masahiro Hamada; Yukiko Nagai; Toshitaka Nakagawa; Naro Ohashi; Daisuke Nakano; Hirofumi Hitomi; Masahito Imanishi
Journal:  J Pharmacol Exp Ther       Date:  2009-11-25       Impact factor: 4.030

10.  Effect of the monocyte chemoattractant protein-1/CC chemokine receptor 2 system on nephrin expression in streptozotocin-treated mice and human cultured podocytes.

Authors:  Elena Tarabra; Sara Giunti; Federica Barutta; Gennaro Salvidio; Davina Burt; Giacomo Deferrari; Roberto Gambino; Daniela Vergola; Silvia Pinach; Paolo Cavallo Perin; Giovanni Camussi; Gabriella Gruden
Journal:  Diabetes       Date:  2009-07-08       Impact factor: 9.461

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