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© Research
Publication : American journal of physiology. Renal physiology

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

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in American journal of physiology. Renal physiology - 06 Jul 2004

Runembert I, Couette S, Federici P, Colucci-Guyon E, Babinet C, Briand P, Friedlander G, Terzi F

Link to Pubmed [PMID] – 15238351

Am. J. Physiol. Renal Physiol. 2004 Nov;287(5):F960-8

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.

http://www.ncbi.nlm.nih.gov/pubmed/15238351