Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Sci. Signal., 18 May 2010
Vol. 3, Issue 122, p. ra39
[DOI: 10.1126/scisignal.2000678]

RESEARCH ARTICLES

Editor's Summary

Podocyte Disruptor
Podocytes are cells with extensions known as foot processes that envelop the capillaries of the glomerulus in the kidney and prevent protein in the bloodstream from entering the urine. In individuals with idiopathic nephrotic syndrome, the podocytes lose their characteristic foot processes (a morphological alteration known as effacement) and protein appears in their urine (a symptom called proteinuria). Zhang et al. found that in some patients with various types of idiopathic nephrotic syndrome, the abundance of a protein known as c-mip was increased in podocytes. Transgenic mice that overexpressed c-mip developed proteinuria and effacement of foot processes. Biochemical analysis indicated that c-mip disrupted the interactions between proteins involved in regulating cytoskeletal reorganization in podocytes. Administration of the bacterial endotoxin lipopolysaccharide (LPS) induces proteinuria in mice, and the authors found that LPS-induced proteinuria was prevented by intravenous injection of a small interfering RNA directed against c-mip. Thus, c-mip may be a potential therapeutic target in the treatment of idiopathic nephrotic syndrome.

Citation: S. y. Zhang, M. Kamal, K. Dahan, A. Pawlak, V. Ory, D. Desvaux, V. Audard, M. Candelier, F. BenMohamed, M. Matignon, C. Christov, X. Decrouy, V. Bernard, G. Mangiapan, P. Lang, G. Guellaën, P. Ronco, D. Sahali, c-mip Impairs Podocyte Proximal Signaling and Induces Heavy Proteinuria. Sci. Signal. 3, ra39 (2010).

Read the Full Text


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Protein A immunoadsorption cannot significantly remove the soluble receptor of urokinase from sera of patients with recurrent focal segmental glomerulosclerosis.
S. Beaudreuil, X. Zhang, F. Kriaa, J. Dantal, H. Francois, A. Vazquez, B. Charpentier, H.-K. Lorenzo, and A. Durrbach (2014)
Nephrol. Dial. Transplant. 29, 458-463
   Abstract »    Full Text »    PDF »
Knockdown of the Hypertension-Associated Gene NOSTRIN Alters Glomerular Barrier Function in Zebrafish (Danio rerio).
T. Kirsch, J. Kaufeld, R. Korstanje, D. M. Hentschel, L. Staggs, F. Bollig, M. Beese, P. Schroder, L. Boehme, H. Haller, et al. (2013)
Hypertension 62, 726-730
   Abstract »    Full Text »    PDF »
Direct Regulation of Nephrin Tyrosine Phosphorylation by Nck Adaptor Proteins.
L. A. New, A. Keyvani Chahi, and N. Jones (2013)
J. Biol. Chem. 288, 1500-1510
   Abstract »    Full Text »    PDF »
Onco-Nephrology: Glomerular Diseases with Cancer.
J.-F. Cambier and P. Ronco (2012)
Clin. J. Am. Soc. Nephrol. 7, 1701-1712
   Abstract »    Full Text »    PDF »
Disruption of cytokeratin-8 interaction with F508del-CFTR corrects its functional defect.
J. Colas, G. Faure, E. Saussereau, S. Trudel, W. M. Rabeh, S. Bitam, I. C. Guerrera, J. Fritsch, I. Sermet-Gaudelus, N. Davezac, et al. (2012)
Hum. Mol. Genet. 21, 623-634
   Abstract »    Full Text »    PDF »

To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882