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Am J Physiol Renal Physiol (July 6, 2004). doi:10.1152/ajprenal.00064.2004
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Submitted on February 27, 2004
Accepted on June 23, 2004

Recovery of sodium-glucose cotransport activity after renal ischemia is impaired in mice lacking vimentin

Isabelle Runembert1, Sylviane Couette1, Pierre Federici2, Emma Colucci-Guyon3, Charles Babinet3, Pascale Briand2, Gerard Friedlander1, and Fabiola Terzi1*

1 Department of Physiologie, Faculte de Medecine Xavier Bichat, INSERM U426, Paris, France
2 Institut Cochin de Genetique Moleculaire, INSERM, Paris, France
3 Institut Pasteur, URA 2578 CNRS, Paris, France

* To whom correspondence should be addressed. E-mail: terzi{at}bichat.inserm.fr.

Vimentin, an intermediate filament protein mainly expressed in mesenchyma-derived cells, is reexpressed in renal tubular epithelial cells under many pathological conditions, characterized by intense cell proliferation. Whether vimentin reexpression is only a marker of cell dedifferentiation or is instrumental in the maintenance of cell structure and/or function is still unknown. Here, we used vimentin knockout mice (Vim-/-) and an experimental model of acute renal injury (30-min bilateral renal ischemia) to explore the role of vimentin. Bilateral renal ischemia induced an initial phase of acute tubular necrosis that did not require vimentin and was similar, in terms of morphological and functional changes, in Vim+/+ and Vim-/- mice. However, vimentin was essential to favor SGLT1 localization to brush border membranes and to restore Na-glucose cotransport activity in regenerating tubular cells. We show that the effect of vimentin inactivation is specific and results in persistent glucosuria. We propose that vimentin is part of a structural network that favors carrier localization to plasma membranes to restore transport activity in injured kidneys.




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