LymphedemaV1, Pmc, Corpus, bibRecord, 002B93

Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow

Identifieur interne : 002B93 ( Pmc/Corpus ); précédent : 002B92; suivant : 002B94

Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow

Auteurs : Sanjeev A. Datar ; Wenhui Gong ; Youping He ; Michael Johengen ; Rebecca J. Kameny ; Gary W. Raff ; Emin Maltepe ; Peter E. Oishi ; Jeffrey R. Fineman

Source :

American Journal of Physiology - Heart and Circulatory Physiology [ 0363-6135 ] ; 2016.

RBID : PMC:4967199

Abstract

Lymphatic endothelial cells, exposed to chronically elevated pulmonary lymph flow in a model of congenital heart disease with increased pulmonary blood flow, demonstrate disrupted nitric oxide (NO) signaling. Specifically, they have altered NO synthase expression and activity that result in increased accumulation of reactive oxygen species and decreased bioavailable NO.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4967199

DOI: 10.1152/ajpheart.00649.2015
PubMed: 27199125
PubMed Central: 4967199

Links to Exploration step

PMC:4967199

Le document en format XML

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<author><name sortKey="Datar, Sanjeev A" sort="Datar, Sanjeev A" uniqKey="Datar S" first="Sanjeev A." last="Datar">Sanjeev A. Datar</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Gong, Wenhui" sort="Gong, Wenhui" uniqKey="Gong W" first="Wenhui" last="Gong">Wenhui Gong</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="He, Youping" sort="He, Youping" uniqKey="He Y" first="Youping" last="He">Youping He</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Johengen, Michael" sort="Johengen, Michael" uniqKey="Johengen M" first="Michael" last="Johengen">Michael Johengen</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kameny, Rebecca J" sort="Kameny, Rebecca J" uniqKey="Kameny R" first="Rebecca J." last="Kameny">Rebecca J. Kameny</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Raff, Gary W" sort="Raff, Gary W" uniqKey="Raff G" first="Gary W." last="Raff">Gary W. Raff</name>
<affiliation><nlm:aff id="aff3">Department of Surgery, University of California, Davis, Davis, California</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Maltepe, Emin" sort="Maltepe, Emin" uniqKey="Maltepe E" first="Emin" last="Maltepe">Emin Maltepe</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Oishi, Peter E" sort="Oishi, Peter E" uniqKey="Oishi P" first="Peter E." last="Oishi">Peter E. Oishi</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
<affiliation><nlm:aff wicri:cut="; and" id="aff2">Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Fineman, Jeffrey R" sort="Fineman, Jeffrey R" uniqKey="Fineman J" first="Jeffrey R." last="Fineman">Jeffrey R. Fineman</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
<affiliation><nlm:aff wicri:cut="; and" id="aff2">Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California</nlm:aff>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow</title>
<author><name sortKey="Datar, Sanjeev A" sort="Datar, Sanjeev A" uniqKey="Datar S" first="Sanjeev A." last="Datar">Sanjeev A. Datar</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Gong, Wenhui" sort="Gong, Wenhui" uniqKey="Gong W" first="Wenhui" last="Gong">Wenhui Gong</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="He, Youping" sort="He, Youping" uniqKey="He Y" first="Youping" last="He">Youping He</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Johengen, Michael" sort="Johengen, Michael" uniqKey="Johengen M" first="Michael" last="Johengen">Michael Johengen</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Kameny, Rebecca J" sort="Kameny, Rebecca J" uniqKey="Kameny R" first="Rebecca J." last="Kameny">Rebecca J. Kameny</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Raff, Gary W" sort="Raff, Gary W" uniqKey="Raff G" first="Gary W." last="Raff">Gary W. Raff</name>
<affiliation><nlm:aff id="aff3">Department of Surgery, University of California, Davis, Davis, California</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Maltepe, Emin" sort="Maltepe, Emin" uniqKey="Maltepe E" first="Emin" last="Maltepe">Emin Maltepe</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Oishi, Peter E" sort="Oishi, Peter E" uniqKey="Oishi P" first="Peter E." last="Oishi">Peter E. Oishi</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
<affiliation><nlm:aff wicri:cut="; and" id="aff2">Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Fineman, Jeffrey R" sort="Fineman, Jeffrey R" uniqKey="Fineman J" first="Jeffrey R." last="Fineman">Jeffrey R. Fineman</name>
<affiliation><nlm:aff id="aff1">Department of Pediatrics, University of California, San Francisco, San Francisco, California;</nlm:aff>
</affiliation>
<affiliation><nlm:aff wicri:cut="; and" id="aff2">Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">American Journal of Physiology - Heart and Circulatory Physiology</title>
<idno type="ISSN">0363-6135</idno>
<idno type="eISSN">1522-1539</idno>
<imprint><date when="2016">2016</date>
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<front><div type="abstract" xml:lang="en"><p><italic>Lymphatic endothelial cells, exposed to chronically elevated pulmonary lymph flow in a model of congenital heart disease with increased pulmonary blood flow, demonstrate disrupted nitric oxide (NO) signaling. Specifically, they have altered NO synthase expression and activity that result in increased accumulation of reactive oxygen species and decreased bioavailable NO</italic>
.</p>
</div>
</front>
</TEI>
<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">Am J Physiol Heart Circ Physiol</journal-id>
<journal-id journal-id-type="iso-abbrev">Am. J. Physiol. Heart Circ. Physiol</journal-id>
<journal-id journal-id-type="hwp">ajpheart</journal-id>
<journal-id journal-id-type="pmc">ajpheart</journal-id>
<journal-id journal-id-type="publisher-id">AJPHEART</journal-id>
<journal-title-group><journal-title>American Journal of Physiology - Heart and Circulatory Physiology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0363-6135</issn>
<issn pub-type="epub">1522-1539</issn>
<publisher><publisher-name>American Physiological Society</publisher-name>
<publisher-loc>Bethesda, MD</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">27199125</article-id>
<article-id pub-id-type="pmc">4967199</article-id>
<article-id pub-id-type="publisher-id">H-00649-2015</article-id>
<article-id pub-id-type="doi">10.1152/ajpheart.00649.2015</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Vascular Biology and Microcirculation</subject>
</subj-group>
</article-categories>
<title-group><article-title>Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow</article-title>
</title-group>
<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Datar</surname>
<given-names>Sanjeev A.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Gong</surname>
<given-names>Wenhui</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>He</surname>
<given-names>Youping</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Johengen</surname>
<given-names>Michael</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kameny</surname>
<given-names>Rebecca J.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Raff</surname>
<given-names>Gary W.</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Maltepe</surname>
<given-names>Emin</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Oishi</surname>
<given-names>Peter E.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Fineman</surname>
<given-names>Jeffrey R.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<aff id="aff1"><sup>1</sup>
Department of Pediatrics, University of California, San Francisco, San Francisco, California;</aff>
<aff id="aff2"><sup>2</sup>
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California; and</aff>
<aff id="aff3"><sup>3</sup>
Department of Surgery, University of California, Davis, Davis, California</aff>
</contrib-group>
<author-notes><corresp id="cor1">Address for reprint requests and other correspondence: S. A. Datar, <addr-line>Dept. of Pediatrics, Univ. of California, San Francisco, San Francisco, CA 94143</addr-line>
 (e-mail: <email>sanjeev.datar@ucsf.edu</email>
).</corresp>
</author-notes>
<pub-date pub-type="epub"><day>13</day>
<month>5</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="ppub"><day>1</day>
<month>7</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>1</day>
<month>7</month>
<year>2017</year>
</pub-date>
<pmc-comment> PMC Release delay is 12 months and 
 						0 days and was based on the . </pmc-comment>
      <volume>311</volume>
<issue>1</issue>
<fpage>H137</fpage>
<lpage>H145</lpage>
<history><date date-type="received"><day>17</day>
<month>8</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>8</day>
<month>4</month>
<year>2016</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2016 the American Physiological Society</copyright-statement>
<copyright-year>2016</copyright-year>
<copyright-holder>American Physiological Society</copyright-holder>
</permissions>
<self-uri content-type="pdf" xlink:href="zh401216000137.pdf"></self-uri>
<abstract abstract-type="precis"><p><italic>Lymphatic endothelial cells, exposed to chronically elevated pulmonary lymph flow in a model of congenital heart disease with increased pulmonary blood flow, demonstrate disrupted nitric oxide (NO) signaling. Specifically, they have altered NO synthase expression and activity that result in increased accumulation of reactive oxygen species and decreased bioavailable NO</italic>
.</p>
</abstract>
<abstract><p>Associated abnormalities of the lymphatic circulation are well described in congenital heart disease. However, their mechanisms remain poorly elucidated. Using a clinically relevant ovine model of a congenital cardiac defect with chronically increased pulmonary blood flow (shunt), we previously demonstrated that exposure to chronically elevated pulmonary lymph flow is associated with: <italic>1</italic>
) decreased bioavailable nitric oxide (NO) in pulmonary lymph; and <italic>2</italic>
) attenuated endothelium-dependent relaxation of thoracic duct rings, suggesting disrupted lymphatic endothelial NO signaling in shunt lambs. To further elucidate the mechanisms responsible for this altered NO signaling, primary lymphatic endothelial cells (LECs) were isolated from the efferent lymphatic of the caudal mediastinal node in 4-wk-old control and shunt lambs. We found that shunt LECs (<italic>n</italic>
 = 3) had decreased bioavailable NO and decreased endothelial nitric oxide synthase (eNOS) mRNA and protein expression compared with control LECs (<italic>n</italic>
 = 3). eNOS activity was also low in shunt LECs, but, interestingly, inducible nitric oxide synthase (iNOS) expression and activity were increased in shunt LECs, as were total cellular nitration, including eNOS-specific nitration, and accumulation of reactive oxygen species (ROS). Pharmacological inhibition of iNOS reduced ROS in shunt LECs to levels measured in control LECs. These data support the conclusion that NOS signaling is disrupted in the lymphatic endothelium of lambs exposed to chronically increased pulmonary blood and lymph flow and may contribute to decreased pulmonary lymphatic bioavailable NO.</p>
</abstract>
<kwd-group><kwd>nitric oxide signaling</kwd>
<kwd>nitric oxide synthase</kwd>
</kwd-group>
<funding-group><award-group id="award1"><funding-source><named-content content-type="funder-id">100000002</named-content>
HHS | National Institutes of Health (NIH)</funding-source>
<award-id>K08HL116763</award-id>
<award-id>HL61284</award-id>
</award-group>
<award-group id="award2"><funding-source><named-content content-type="funder-id">100000968</named-content>
American Heart Association (AHA)</funding-source>
<award-id>12BGIA11540021</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
</pmc>
</record>

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Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow

Disrupted NOS signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow

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