Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL

Article Article scientifique Article Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL eng 2003 author Bustamante Mauro author Roger Frank 507676 author Bochaton-Piallat Marie-Luce 0000-0001-8408-8932 23951 Marie-Luce Piallat author Gabbiani Giulio 24889 author Martin Pierre-Yves 65591 author Feraille Eric 27356 F336-347 10.1152/ajprenal.00003.2003 12724128 0363-6127 http://ajprenal.physiology.org/cgi/reprint/285/2/F336.pdf The kidney medulla is physiologically exposed to variations in extracellular osmolality. In response to hypertonic cell shrinkage, cells of the rat kidney medullary thick ascending limb of Henle's loop undergo p38 kinase-dependent regulatory volume increase (RVI). In the present study, we investigated the role of actin cytoskeleton reorganization in this process. Addition of hyperosmotic NaCl or sucrose, which activates MAP kinases and reduces cellular volume, induced a sustained actin polymerization occurring after 10 min and concurrently with RVI. In contrast, hyperosmotic urea, which does not modify MAP kinase activity and cellular volume, did not induce sustained actin polymerization. Fluorescence microscopy revealed that hyperosmotic NaCl and sucrose, but not urea, induced the redistribution of F-actin from a dense cortical ring to a diffuse network of actin bundles. Stabilization of actin filaments by jasplakinolide and inhibition of the generation of new actin filaments by swinholide A prevented RVI, whereas depolymerization of actin filaments by latrunculin B attenuated cell shrinkage and enhanced RVI. These actin-interfering drugs did not alter extracellular regulated kinase and p38 kinase activation under hypertonic conditions. Similar to swinholide A, inhibiting p38 kinase with SB-203580 abolished sustained actin polymerization, actin redistribution, and decreased RVI efficacy. We therefore propose that in rat kidney the medullary thick ascending limb of Henle's loop exposed to extracellular hypertonicity, p38 kinase activation induces depolymerization of the F-actin cortical ring and polymerization of a dense diffuse F-actin network that both contribute to increase RVI efficacy. Actins/metabolism Animals Enzyme Inhibitors/pharmacology Imidazoles/pharmacology Loop of Henle/ enzymology Male Marine Toxins/pharmacology Microfilaments/ metabolism Mitogen-Activated Protein Kinases/antagonists & inhibitors/ metabolism Osmotic Pressure Polymers Pyridines/pharmacology Rats Rats, Wistar Saline Solution, Hypertonic/pharmacology Sucrose/pharmacology Urea/pharmacology Water-Electrolyte Balance/drug effects/ physiology P38 Mitogen-Activated Protein Kinases Dewey 616.07 137 Département de pathologie et immunologie 21F false American journal of physiology. Renal, fluid and electrolyte physiology 285 2 22dfc2a9-367c-4afa-ba79-06555faf1126 Article Restricted file1.pdf 643684 application/pdf restrictedAccess Faculté de médecine / Section de médecine fondamentale / Département de pathologie et immunologie

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Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL	American journal of physiology. Renal, fluid and electrolyte physiology			2003	641	0

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Roger, Frank