ROCK and cAMP Promote Lymphatic Endothelial Cell Barrier Integrity and Modulate Histamine and Thrombin-Induced Barrier Dysfunction
Identifieur interne : 003062 ( Pmc/Corpus ); précédent : 003061; suivant : 003063ROCK and cAMP Promote Lymphatic Endothelial Cell Barrier Integrity and Modulate Histamine and Thrombin-Induced Barrier Dysfunction
Auteurs : Jerome W. BreslinSource :
- Lymphatic Research and Biology [ 1539-6851 ] ; 2011.
Abstract
There is recent evidence that inflammatory signals can modulate lymphatic vessel permeability, but current understanding of the mechanisms regulating lymphatic endothelial barrier function is limited. The objectives of this study were to 1) investigate whether inflammatory mediators that increase microvascular permeability also cause barrier dysfunction of lymphatic endothelial cell monolayers, and 2) determine the roles of signaling pathways that affect intercellular junctions and cell contraction in lymphatic endothelial barrier function.
Transendothelial electrical resistance (TER) of confluent adult human microlymphatic endothelial cells of dermal origin (HMLEC-d) served as an indicator of lymphatic endothelial barrier function. Human umbilical vein endothelial cells (HUVEC) were used to model blood-tissue barrier function. The inflammatory mediators histamine and thrombin each caused a decrease in TER of HMLEC-d and HUVEC monolayers, with notable differences between the two cell types. Treatment with 8-Br-cAMP enhanced HMLEC-d barrier function, which limited histamine and thrombin-induced decreases in TER. Blockade of myosin light chain kinase (MLCK) with ML-7 did not affect histamine or thrombin-induced decreases in TER. Treatment with the Rho kinase (ROCK) inhibitor Y-27632 caused a decrease in HMLEC-d barrier function.
These data show that inflammatory mediators can cause lymphatic endothelial barrier dysfunction, although the responses are not identical to those seen with blood endothelial cells. ROCK and cAMP both promote lymphatic endothelial barrier function, however ROCK appears to also serve as a mediator of histamine and thrombin-induced barrier dysfunction.
Url:
DOI: 10.1089/lrb.2010.0016
PubMed: 21417762
PubMed Central: 3060730
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PMC:3060730Le document en format XML
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<author><name sortKey="Breslin, Jerome W" sort="Breslin, Jerome W" uniqKey="Breslin J" first="Jerome W." last="Breslin">Jerome W. Breslin</name>
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<series><title level="j">Lymphatic Research and Biology</title>
<idno type="ISSN">1539-6851</idno>
<idno type="eISSN">1557-8585</idno>
<imprint><date when="2011">2011</date>
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<front><div type="abstract" xml:lang="en"><title>Abstract</title>
<sec><title>Background</title>
<p>There is recent evidence that inflammatory signals can modulate lymphatic vessel permeability, but current understanding of the mechanisms regulating lymphatic endothelial barrier function is limited. The objectives of this study were to 1) investigate whether inflammatory mediators that increase microvascular permeability also cause barrier dysfunction of lymphatic endothelial cell monolayers, and 2) determine the roles of signaling pathways that affect intercellular junctions and cell contraction in lymphatic endothelial barrier function.</p>
</sec>
<sec><title>Methods and Results</title>
<p>Transendothelial electrical resistance (TER) of confluent adult human microlymphatic endothelial cells of dermal origin (HMLEC-d) served as an indicator of lymphatic endothelial barrier function. Human umbilical vein endothelial cells (HUVEC) were used to model blood-tissue barrier function. The inflammatory mediators histamine and thrombin each caused a decrease in TER of HMLEC-d and HUVEC monolayers, with notable differences between the two cell types. Treatment with 8-Br-cAMP enhanced HMLEC-d barrier function, which limited histamine and thrombin-induced decreases in TER. Blockade of myosin light chain kinase (MLCK) with ML-7 did not affect histamine or thrombin-induced decreases in TER. Treatment with the Rho kinase (ROCK) inhibitor Y-27632 caused a decrease in HMLEC-d barrier function.</p>
</sec>
<sec><title>Conclusions</title>
<p>These data show that inflammatory mediators can cause lymphatic endothelial barrier dysfunction, although the responses are not identical to those seen with blood endothelial cells. ROCK and cAMP both promote lymphatic endothelial barrier function, however ROCK appears to also serve as a mediator of histamine and thrombin-induced barrier dysfunction.</p>
</sec>
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<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Lymphat Res Biol</journal-id>
<journal-id journal-id-type="publisher-id">lrb</journal-id>
<journal-title-group><journal-title>Lymphatic Research and Biology</journal-title>
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<issn pub-type="ppub">1539-6851</issn>
<issn pub-type="epub">1557-8585</issn>
<publisher><publisher-name>Mary Ann Liebert, Inc.</publisher-name>
<publisher-loc>140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA</publisher-loc>
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<article-id pub-id-type="pmc">3060730</article-id>
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<article-id pub-id-type="doi">10.1089/lrb.2010.0016</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Original Articles</subject>
</subj-group>
</article-categories>
<title-group><article-title>ROCK and cAMP Promote Lymphatic Endothelial Cell Barrier Integrity and Modulate Histamine and Thrombin-Induced Barrier Dysfunction</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Breslin</surname>
<given-names>Jerome W.</given-names>
</name>
<degrees>Ph.D.</degrees>
</contrib>
<aff id="aff1">Department of Physiology, School of Medicine,<institution>Louisiana State University Health Sciences Center</institution>
, New Orleans, Louisiana.</aff>
</contrib-group>
<author-notes><corresp>Address correspondence to: <italic>Jerome W. Breslin, Ph.D., Department of Physiology, LSUHSC-NO School of Medicine, 1901 Perdido St Box P7-3, New Orleans, LA 70112. E-mail:</italic>
<email xlink:href="mailto:jbresl@lsuhsc.edu">jbresl@lsuhsc.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>3</month>
<year>2011</year>
<pmc-comment>string-date: March 2011</pmc-comment>
</pub-date>
<volume>9</volume>
<issue>1</issue>
<fpage>3</fpage>
<lpage>11</lpage>
<permissions><copyright-statement>Copyright 2011, Mary Ann Liebert, Inc.</copyright-statement>
</permissions>
<self-uri xlink:type="simple" xlink:href="lrb.2010.0016.pdf"></self-uri>
<abstract><title>Abstract</title>
<sec><title>Background</title>
<p>There is recent evidence that inflammatory signals can modulate lymphatic vessel permeability, but current understanding of the mechanisms regulating lymphatic endothelial barrier function is limited. The objectives of this study were to 1) investigate whether inflammatory mediators that increase microvascular permeability also cause barrier dysfunction of lymphatic endothelial cell monolayers, and 2) determine the roles of signaling pathways that affect intercellular junctions and cell contraction in lymphatic endothelial barrier function.</p>
</sec>
<sec><title>Methods and Results</title>
<p>Transendothelial electrical resistance (TER) of confluent adult human microlymphatic endothelial cells of dermal origin (HMLEC-d) served as an indicator of lymphatic endothelial barrier function. Human umbilical vein endothelial cells (HUVEC) were used to model blood-tissue barrier function. The inflammatory mediators histamine and thrombin each caused a decrease in TER of HMLEC-d and HUVEC monolayers, with notable differences between the two cell types. Treatment with 8-Br-cAMP enhanced HMLEC-d barrier function, which limited histamine and thrombin-induced decreases in TER. Blockade of myosin light chain kinase (MLCK) with ML-7 did not affect histamine or thrombin-induced decreases in TER. Treatment with the Rho kinase (ROCK) inhibitor Y-27632 caused a decrease in HMLEC-d barrier function.</p>
</sec>
<sec><title>Conclusions</title>
<p>These data show that inflammatory mediators can cause lymphatic endothelial barrier dysfunction, although the responses are not identical to those seen with blood endothelial cells. ROCK and cAMP both promote lymphatic endothelial barrier function, however ROCK appears to also serve as a mediator of histamine and thrombin-induced barrier dysfunction.</p>
</sec>
</abstract>
<counts><fig-count count="7"></fig-count>
<ref-count count="45"></ref-count>
<page-count count="9"></page-count>
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