Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL
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 inves...
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Veröffentlicht in: | American journal of physiology. Renal physiology 2003-08, Vol.285 (2), p.F336-F347 |
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container_title | American journal of physiology. Renal physiology |
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creator | Bustamante, Mauro Roger, Frank Bochaton-Piallat, Marie-Luce Gabbiani, Giulio Martin, Pierre-Yves Feraille, Eric |
description | 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. |
doi_str_mv | 10.1152/ajprenal.00003.2003 |
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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.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00003.2003</identifier><identifier>PMID: 12724128</identifier><language>eng</language><publisher>United States</publisher><subject>Actin Cytoskeleton - metabolism ; Actins - metabolism ; Animals ; Enzyme Inhibitors - pharmacology ; Imidazoles - pharmacology ; Loop of Henle - enzymology ; Male ; Marine Toxins - pharmacology ; Mitogen-Activated Protein Kinases - antagonists & inhibitors ; Mitogen-Activated Protein Kinases - metabolism ; Osmotic Pressure ; p38 Mitogen-Activated Protein Kinases ; Polymers ; Pyridines - pharmacology ; Rats ; Rats, Wistar ; Saline Solution, Hypertonic - pharmacology ; Sucrose - pharmacology ; Urea - pharmacology ; Water-Electrolyte Balance - drug effects ; Water-Electrolyte Balance - physiology</subject><ispartof>American journal of physiology. Renal physiology, 2003-08, Vol.285 (2), p.F336-F347</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-127a2c7d2c8433376dbbb7ed2c0116b86c71b34ef841a3dd38a8c18ba7c6d0633</citedby><cites>FETCH-LOGICAL-c391t-127a2c7d2c8433376dbbb7ed2c0116b86c71b34ef841a3dd38a8c18ba7c6d0633</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12724128$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bustamante, Mauro</creatorcontrib><creatorcontrib>Roger, Frank</creatorcontrib><creatorcontrib>Bochaton-Piallat, Marie-Luce</creatorcontrib><creatorcontrib>Gabbiani, Giulio</creatorcontrib><creatorcontrib>Martin, Pierre-Yves</creatorcontrib><creatorcontrib>Feraille, Eric</creatorcontrib><title>Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>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.</description><subject>Actin Cytoskeleton - metabolism</subject><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Imidazoles - pharmacology</subject><subject>Loop of Henle - enzymology</subject><subject>Male</subject><subject>Marine Toxins - pharmacology</subject><subject>Mitogen-Activated Protein Kinases - antagonists & inhibitors</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>Osmotic Pressure</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Polymers</subject><subject>Pyridines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Saline Solution, Hypertonic - pharmacology</subject><subject>Sucrose - pharmacology</subject><subject>Urea - pharmacology</subject><subject>Water-Electrolyte Balance - drug effects</subject><subject>Water-Electrolyte Balance - physiology</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkG1LwzAQx4Mobk4_gSD5Ap29pGuzl2PoFCaCTPBdSZPbzNamJcmUfnszN_Fe3AN3_-PuR8gtpGOACbuX286hlfU4jcbHLLozMowdlkCW5-cxn3JIxKT4GJAr77dxDIDBJRkAK1gGTAyJf8PNvpahdT39aut9g9RY5VD6mHgqvW-VkQE1_Tbhk3Zc0J2xsZto7NBqtIFKFYylqg-t32GNobXUYdNqrI3dxHXUyRBV2mJPX1az5TW5WMva480pjsj748Nq_pQsXxfP89kyUXwKIYlHSqYKzZTIOOdFrquqKjDW8Y28ErkqoOIZrkUGkmvNhRQKRCULles053xE-HGvcq33Dtdl50wjXV9CWh4Qln8Iy1-E5QFhVN0dVd2-alD_a07M-A8CtHEZ</recordid><startdate>200308</startdate><enddate>200308</enddate><creator>Bustamante, Mauro</creator><creator>Roger, Frank</creator><creator>Bochaton-Piallat, Marie-Luce</creator><creator>Gabbiani, Giulio</creator><creator>Martin, Pierre-Yves</creator><creator>Feraille, Eric</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>200308</creationdate><title>Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL</title><author>Bustamante, Mauro ; Roger, Frank ; Bochaton-Piallat, Marie-Luce ; Gabbiani, Giulio ; Martin, Pierre-Yves ; Feraille, Eric</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-127a2c7d2c8433376dbbb7ed2c0116b86c71b34ef841a3dd38a8c18ba7c6d0633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Actin Cytoskeleton - metabolism</topic><topic>Actins - metabolism</topic><topic>Animals</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Imidazoles - pharmacology</topic><topic>Loop of Henle - enzymology</topic><topic>Male</topic><topic>Marine Toxins - pharmacology</topic><topic>Mitogen-Activated Protein Kinases - antagonists & inhibitors</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>Osmotic Pressure</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Polymers</topic><topic>Pyridines - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Saline Solution, Hypertonic - pharmacology</topic><topic>Sucrose - pharmacology</topic><topic>Urea - pharmacology</topic><topic>Water-Electrolyte Balance - drug effects</topic><topic>Water-Electrolyte Balance - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bustamante, Mauro</creatorcontrib><creatorcontrib>Roger, Frank</creatorcontrib><creatorcontrib>Bochaton-Piallat, Marie-Luce</creatorcontrib><creatorcontrib>Gabbiani, Giulio</creatorcontrib><creatorcontrib>Martin, Pierre-Yves</creatorcontrib><creatorcontrib>Feraille, Eric</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bustamante, Mauro</au><au>Roger, Frank</au><au>Bochaton-Piallat, Marie-Luce</au><au>Gabbiani, Giulio</au><au>Martin, Pierre-Yves</au><au>Feraille, Eric</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2003-08</date><risdate>2003</risdate><volume>285</volume><issue>2</issue><spage>F336</spage><epage>F347</epage><pages>F336-F347</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>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.</abstract><cop>United States</cop><pmid>12724128</pmid><doi>10.1152/ajprenal.00003.2003</doi></addata></record> |
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subjects | Actin Cytoskeleton - metabolism Actins - metabolism Animals Enzyme Inhibitors - pharmacology Imidazoles - pharmacology Loop of Henle - enzymology Male Marine Toxins - pharmacology Mitogen-Activated Protein Kinases - antagonists & inhibitors Mitogen-Activated Protein Kinases - metabolism Osmotic Pressure p38 Mitogen-Activated Protein Kinases Polymers Pyridines - pharmacology Rats Rats, Wistar Saline Solution, Hypertonic - pharmacology Sucrose - pharmacology Urea - pharmacology Water-Electrolyte Balance - drug effects Water-Electrolyte Balance - physiology |
title | Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL |
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