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

¹Institut National de la Santé et de la Recherche Médicale Unitè 426 Department of Physiologie, Faculté de Médecine Xavier Bichat, 75870 Paris, Cedex 18; ²Institut Cochin de Génétique Moléculaire, 75014 Paris; and ³Unité de Recherche Associée 2578 Centre National de la Recherche Scientifique, Institut Pasteur, 75015 Paris, France

Submitted 27 February 2004 ; accepted in final form 23 June 2004

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 Na-glucose cotransporter 1 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.

recovery; sodium-glucose cotransporter 1; glucosuria

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