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Shock-induced stress induces loss of microvascular endothelial Tie2 in the kidney which is not associated with reduced glomerular barrier function
Both hemorrhagic shock and endotoxemia induce a pronounced vascular activation in the kidney which coincides with albuminuria and glomerular barrier dysfunction. We hypothesized that changes in Tie2, a vascular restricted receptor tyrosine kinase shown to control microvascular integrity and endothel...
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| Published in: | American journal of physiology. Renal physiology 2009-08, Vol.297 (2), p.F272-F281 |
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| container_title | American journal of physiology. Renal physiology |
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| creator | van Meurs, Matijs Kurniati, Neng F Wulfert, Francis M Asgeirsdottir, Sigridur A de Graaf, Inge A Satchell, Simon C Mathieson, Peter W Jongman, Rianne M Kümpers, Philipp Zijlstra, Jan G Heeringa, Peter Molema, Grietje |
| description | Both hemorrhagic shock and endotoxemia induce a pronounced vascular activation in the kidney which coincides with albuminuria and glomerular barrier dysfunction. We hypothesized that changes in Tie2, a vascular restricted receptor tyrosine kinase shown to control microvascular integrity and endothelial inflammation, underlie this loss of glomerular barrier function. In healthy murine and human kidney, Tie2 is heterogeneously expressed in all microvascular beds, although to different extents. In mice subjected to hemorrhagic and septic shock, Tie2 mRNA and protein were rapidly, and temporarily, lost from the renal microvasculature, and normalized within 24 h after initiation of the shock insult. The loss of Tie2 protein could not be attributed to shedding as both in mice and healthy volunteers subjected to endotoxemia, sTie2 levels in the systemic circulation did not change. In an attempt to identify the molecular control of Tie2, we activated glomerular endothelial cell cultures and human kidney slices in vitro with LPS or TNF-alpha, but did not observe a change in Tie2 mRNA levels. In parallel to the loss of Tie2 in vivo, an overt influx of neutrophils in the glomerular compartment, which coincided with proteinuria, was seen. As neutrophil-endothelial cell interactions may play a role in endothelial adaptation to shock, and these effects cannot be mimicked in vitro, we depleted neutrophils before shock induction. While this neutrophil depletion abolished proteinuria, Tie2 was not rescued, implying that Tie2 may not be a major factor controlling maintenance of the glomerular filtration barrier in this model. |
| doi_str_mv | 10.1152/ajprenal.00137.2009 |
| format | article |
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We hypothesized that changes in Tie2, a vascular restricted receptor tyrosine kinase shown to control microvascular integrity and endothelial inflammation, underlie this loss of glomerular barrier function. In healthy murine and human kidney, Tie2 is heterogeneously expressed in all microvascular beds, although to different extents. In mice subjected to hemorrhagic and septic shock, Tie2 mRNA and protein were rapidly, and temporarily, lost from the renal microvasculature, and normalized within 24 h after initiation of the shock insult. The loss of Tie2 protein could not be attributed to shedding as both in mice and healthy volunteers subjected to endotoxemia, sTie2 levels in the systemic circulation did not change. In an attempt to identify the molecular control of Tie2, we activated glomerular endothelial cell cultures and human kidney slices in vitro with LPS or TNF-alpha, but did not observe a change in Tie2 mRNA levels. In parallel to the loss of Tie2 in vivo, an overt influx of neutrophils in the glomerular compartment, which coincided with proteinuria, was seen. As neutrophil-endothelial cell interactions may play a role in endothelial adaptation to shock, and these effects cannot be mimicked in vitro, we depleted neutrophils before shock induction. While this neutrophil depletion abolished proteinuria, Tie2 was not rescued, implying that Tie2 may not be a major factor controlling maintenance of the glomerular filtration barrier in this model.</description><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.00137.2009</identifier><identifier>PMID: 19515812</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Aged ; Albuminuria - metabolism ; Albuminuria - physiopathology ; Animals ; Capillary Permeability ; Cell culture ; Cell Line ; Disease Models, Animal ; Down-Regulation ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - physiopathology ; Gene expression ; Glomerular Filtration Rate ; Humans ; In Vitro Techniques ; Kidney - blood supply ; Kidney - metabolism ; Kidney - physiopathology ; Kidneys ; Kinases ; Lipopolysaccharides ; Male ; Mice ; Mice, Inbred C57BL ; Microvessels - metabolism ; Middle Aged ; Neutrophils - metabolism ; Physiology ; Proteins ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor Protein-Tyrosine Kinases - metabolism ; Receptor, TIE-2 - genetics ; Receptor, TIE-2 - metabolism ; Ribonucleic acid ; RNA ; RNA, Messenger - metabolism ; Rodents ; Shock, Hemorrhagic - metabolism ; Shock, Hemorrhagic - physiopathology ; Shock, Septic - chemically induced ; Shock, Septic - metabolism ; Shock, Septic - physiopathology ; Time Factors ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>American journal of physiology. Renal physiology, 2009-08, Vol.297 (2), p.F272-F281</ispartof><rights>Copyright American Physiological Society Aug 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c369t-1146d878a893c194381921f9e95fa5ff03c6cd3162eb758c0c836573c361928e3</citedby><cites>FETCH-LOGICAL-c369t-1146d878a893c194381921f9e95fa5ff03c6cd3162eb758c0c836573c361928e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19515812$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Meurs, Matijs</creatorcontrib><creatorcontrib>Kurniati, Neng F</creatorcontrib><creatorcontrib>Wulfert, Francis M</creatorcontrib><creatorcontrib>Asgeirsdottir, Sigridur A</creatorcontrib><creatorcontrib>de Graaf, Inge A</creatorcontrib><creatorcontrib>Satchell, Simon C</creatorcontrib><creatorcontrib>Mathieson, Peter W</creatorcontrib><creatorcontrib>Jongman, Rianne M</creatorcontrib><creatorcontrib>Kümpers, Philipp</creatorcontrib><creatorcontrib>Zijlstra, Jan G</creatorcontrib><creatorcontrib>Heeringa, Peter</creatorcontrib><creatorcontrib>Molema, Grietje</creatorcontrib><title>Shock-induced stress induces loss of microvascular endothelial Tie2 in the kidney which is not associated with reduced glomerular barrier function</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol Renal Physiol</addtitle><description>Both hemorrhagic shock and endotoxemia induce a pronounced vascular activation in the kidney which coincides with albuminuria and glomerular barrier dysfunction. We hypothesized that changes in Tie2, a vascular restricted receptor tyrosine kinase shown to control microvascular integrity and endothelial inflammation, underlie this loss of glomerular barrier function. In healthy murine and human kidney, Tie2 is heterogeneously expressed in all microvascular beds, although to different extents. In mice subjected to hemorrhagic and septic shock, Tie2 mRNA and protein were rapidly, and temporarily, lost from the renal microvasculature, and normalized within 24 h after initiation of the shock insult. The loss of Tie2 protein could not be attributed to shedding as both in mice and healthy volunteers subjected to endotoxemia, sTie2 levels in the systemic circulation did not change. In an attempt to identify the molecular control of Tie2, we activated glomerular endothelial cell cultures and human kidney slices in vitro with LPS or TNF-alpha, but did not observe a change in Tie2 mRNA levels. In parallel to the loss of Tie2 in vivo, an overt influx of neutrophils in the glomerular compartment, which coincided with proteinuria, was seen. As neutrophil-endothelial cell interactions may play a role in endothelial adaptation to shock, and these effects cannot be mimicked in vitro, we depleted neutrophils before shock induction. While this neutrophil depletion abolished proteinuria, Tie2 was not rescued, implying that Tie2 may not be a major factor controlling maintenance of the glomerular filtration barrier in this model.</description><subject>Aged</subject><subject>Albuminuria - metabolism</subject><subject>Albuminuria - physiopathology</subject><subject>Animals</subject><subject>Capillary Permeability</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Gene expression</subject><subject>Glomerular Filtration Rate</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Kidney - blood supply</subject><subject>Kidney - metabolism</subject><subject>Kidney - physiopathology</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Microvessels - metabolism</subject><subject>Middle Aged</subject><subject>Neutrophils - metabolism</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor Protein-Tyrosine Kinases - metabolism</subject><subject>Receptor, TIE-2 - genetics</subject><subject>Receptor, TIE-2 - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Shock, Hemorrhagic - metabolism</subject><subject>Shock, Hemorrhagic - physiopathology</subject><subject>Shock, Septic - chemically induced</subject><subject>Shock, Septic - metabolism</subject><subject>Shock, Septic - physiopathology</subject><subject>Time Factors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1931-857X</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNpFUctOwzAQtBCIR-ELkJDFPcVrN4l9RIiXVIkDReIWuc6GuCRxsRMqfoMvxiVFnHZHnpmVZwg5BzYFSPmVXq09drqZMgYin3LG1B45ji88gVmW7cddCUhkmr8ekZMQViwSgcMhOQKVQiqBH5Pv59qZ98R25WCwpKH3GAIdYaCNi8BVtLXGu08dzNBoT7ErXV9jY3VDFxZ5pNOI6bstO_yim9qamtpAO9dTHYIzVvfRe2P7mnocD701rkX_a7fU3lv0tBo601vXnZKDSjcBz3ZzQl7ubhc3D8n86f7x5nqeGJGpPoH4yVLmUkslDKiZkKA4VApVWum0qpgwmSkFZByXeSoNM1JkaS6iOhIligm5HH3X3n0MGPpi5QYfAw0FFzEpxWezSBIjKQYQgseqWHvbav9VACu2NRR_NRS_NRTbGqLqYmc9LFss_zW73MUPYdmHxA</recordid><startdate>20090801</startdate><enddate>20090801</enddate><creator>van Meurs, Matijs</creator><creator>Kurniati, Neng F</creator><creator>Wulfert, Francis M</creator><creator>Asgeirsdottir, Sigridur A</creator><creator>de Graaf, Inge A</creator><creator>Satchell, Simon C</creator><creator>Mathieson, Peter W</creator><creator>Jongman, Rianne M</creator><creator>Kümpers, Philipp</creator><creator>Zijlstra, Jan G</creator><creator>Heeringa, Peter</creator><creator>Molema, Grietje</creator><general>American Physiological Society</general><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>20090801</creationdate><title>Shock-induced stress induces loss of microvascular endothelial Tie2 in the kidney which is not associated with reduced glomerular barrier function</title><author>van Meurs, Matijs ; Kurniati, Neng F ; Wulfert, Francis M ; Asgeirsdottir, Sigridur A ; de Graaf, Inge A ; Satchell, Simon C ; Mathieson, Peter W ; Jongman, Rianne M ; Kümpers, Philipp ; Zijlstra, Jan G ; Heeringa, Peter ; Molema, Grietje</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c369t-1146d878a893c194381921f9e95fa5ff03c6cd3162eb758c0c836573c361928e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Aged</topic><topic>Albuminuria - metabolism</topic><topic>Albuminuria - physiopathology</topic><topic>Animals</topic><topic>Capillary Permeability</topic><topic>Cell culture</topic><topic>Cell Line</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Gene expression</topic><topic>Glomerular Filtration Rate</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Kidney - blood supply</topic><topic>Kidney - metabolism</topic><topic>Kidney - physiopathology</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Microvessels - metabolism</topic><topic>Middle Aged</topic><topic>Neutrophils - metabolism</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Receptor, TIE-2 - genetics</topic><topic>Receptor, TIE-2 - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Shock, Hemorrhagic - metabolism</topic><topic>Shock, Hemorrhagic - physiopathology</topic><topic>Shock, Septic - chemically induced</topic><topic>Shock, Septic - metabolism</topic><topic>Shock, Septic - physiopathology</topic><topic>Time Factors</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Meurs, Matijs</creatorcontrib><creatorcontrib>Kurniati, Neng F</creatorcontrib><creatorcontrib>Wulfert, Francis M</creatorcontrib><creatorcontrib>Asgeirsdottir, Sigridur A</creatorcontrib><creatorcontrib>de Graaf, Inge A</creatorcontrib><creatorcontrib>Satchell, Simon C</creatorcontrib><creatorcontrib>Mathieson, Peter W</creatorcontrib><creatorcontrib>Jongman, Rianne M</creatorcontrib><creatorcontrib>Kümpers, Philipp</creatorcontrib><creatorcontrib>Zijlstra, Jan G</creatorcontrib><creatorcontrib>Heeringa, Peter</creatorcontrib><creatorcontrib>Molema, Grietje</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>van Meurs, Matijs</au><au>Kurniati, Neng F</au><au>Wulfert, Francis M</au><au>Asgeirsdottir, Sigridur A</au><au>de Graaf, Inge A</au><au>Satchell, Simon C</au><au>Mathieson, Peter W</au><au>Jongman, Rianne M</au><au>Kümpers, Philipp</au><au>Zijlstra, Jan G</au><au>Heeringa, Peter</au><au>Molema, Grietje</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Shock-induced stress induces loss of microvascular endothelial Tie2 in the kidney which is not associated with reduced glomerular barrier function</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol Renal Physiol</addtitle><date>2009-08-01</date><risdate>2009</risdate><volume>297</volume><issue>2</issue><spage>F272</spage><epage>F281</epage><pages>F272-F281</pages><issn>1931-857X</issn><eissn>1522-1466</eissn><abstract>Both hemorrhagic shock and endotoxemia induce a pronounced vascular activation in the kidney which coincides with albuminuria and glomerular barrier dysfunction. We hypothesized that changes in Tie2, a vascular restricted receptor tyrosine kinase shown to control microvascular integrity and endothelial inflammation, underlie this loss of glomerular barrier function. In healthy murine and human kidney, Tie2 is heterogeneously expressed in all microvascular beds, although to different extents. In mice subjected to hemorrhagic and septic shock, Tie2 mRNA and protein were rapidly, and temporarily, lost from the renal microvasculature, and normalized within 24 h after initiation of the shock insult. The loss of Tie2 protein could not be attributed to shedding as both in mice and healthy volunteers subjected to endotoxemia, sTie2 levels in the systemic circulation did not change. In an attempt to identify the molecular control of Tie2, we activated glomerular endothelial cell cultures and human kidney slices in vitro with LPS or TNF-alpha, but did not observe a change in Tie2 mRNA levels. In parallel to the loss of Tie2 in vivo, an overt influx of neutrophils in the glomerular compartment, which coincided with proteinuria, was seen. As neutrophil-endothelial cell interactions may play a role in endothelial adaptation to shock, and these effects cannot be mimicked in vitro, we depleted neutrophils before shock induction. While this neutrophil depletion abolished proteinuria, Tie2 was not rescued, implying that Tie2 may not be a major factor controlling maintenance of the glomerular filtration barrier in this model.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>19515812</pmid><doi>10.1152/ajprenal.00137.2009</doi></addata></record> |
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| identifier | ISSN: 1931-857X |
| ispartof | American journal of physiology. Renal physiology, 2009-08, Vol.297 (2), p.F272-F281 |
| issn | 1931-857X 1522-1466 |
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| subjects | Aged Albuminuria - metabolism Albuminuria - physiopathology Animals Capillary Permeability Cell culture Cell Line Disease Models, Animal Down-Regulation Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Gene expression Glomerular Filtration Rate Humans In Vitro Techniques Kidney - blood supply Kidney - metabolism Kidney - physiopathology Kidneys Kinases Lipopolysaccharides Male Mice Mice, Inbred C57BL Microvessels - metabolism Middle Aged Neutrophils - metabolism Physiology Proteins Receptor Protein-Tyrosine Kinases - genetics Receptor Protein-Tyrosine Kinases - metabolism Receptor, TIE-2 - genetics Receptor, TIE-2 - metabolism Ribonucleic acid RNA RNA, Messenger - metabolism Rodents Shock, Hemorrhagic - metabolism Shock, Hemorrhagic - physiopathology Shock, Septic - chemically induced Shock, Septic - metabolism Shock, Septic - physiopathology Time Factors Tumor Necrosis Factor-alpha - metabolism |
| title | Shock-induced stress induces loss of microvascular endothelial Tie2 in the kidney which is not associated with reduced glomerular barrier function |
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