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<title xml:lang="en">Thrombospondin-1 and CD47 Regulation of Cardiac, Pulmonary and Vascular Responses in Health and Disease</title>
<author>
<name sortKey="Rogers, Natasha M" sort="Rogers, Natasha M" uniqKey="Rogers N" first="Natasha M." last="Rogers">Natasha M. Rogers</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A4">Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Sharifi Sanjani, Maryam" sort="Sharifi Sanjani, Maryam" uniqKey="Sharifi Sanjani M" first="Maryam" last="Sharifi-Sanjani">Maryam Sharifi-Sanjani</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Csanyi, Gabor" sort="Csanyi, Gabor" uniqKey="Csanyi G" first="Gábor" last="Csányi">Gábor Csányi</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A3">Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Pagano, Patrick J" sort="Pagano, Patrick J" uniqKey="Pagano P" first="Patrick J." last="Pagano">Patrick J. Pagano</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A3">Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Isenberg, Jeffrey S" sort="Isenberg, Jeffrey S" uniqKey="Isenberg J" first="Jeffrey S." last="Isenberg">Jeffrey S. Isenberg</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A2">Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A3">Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A4">Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
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<idno type="doi">10.1016/j.matbio.2014.01.002</idno>
<date when="2014">2014</date>
<idno type="wicri:Area/Pmc/Corpus">001874</idno>
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<title xml:lang="en" level="a" type="main">Thrombospondin-1 and CD47 Regulation of Cardiac, Pulmonary and Vascular Responses in Health and Disease</title>
<author>
<name sortKey="Rogers, Natasha M" sort="Rogers, Natasha M" uniqKey="Rogers N" first="Natasha M." last="Rogers">Natasha M. Rogers</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A4">Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Sharifi Sanjani, Maryam" sort="Sharifi Sanjani, Maryam" uniqKey="Sharifi Sanjani M" first="Maryam" last="Sharifi-Sanjani">Maryam Sharifi-Sanjani</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Csanyi, Gabor" sort="Csanyi, Gabor" uniqKey="Csanyi G" first="Gábor" last="Csányi">Gábor Csányi</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A3">Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Pagano, Patrick J" sort="Pagano, Patrick J" uniqKey="Pagano P" first="Patrick J." last="Pagano">Patrick J. Pagano</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A3">Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
</author>
<author>
<name sortKey="Isenberg, Jeffrey S" sort="Isenberg, Jeffrey S" uniqKey="Isenberg J" first="Jeffrey S." last="Isenberg">Jeffrey S. Isenberg</name>
<affiliation>
<nlm:aff id="A1">Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A2">Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A3">Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
<affiliation>
<nlm:aff id="A4">Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</nlm:aff>
</affiliation>
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<title level="j">Matrix biology : journal of the International Society for Matrix Biology</title>
<idno type="ISSN">0945-053X</idno>
<idno type="eISSN">1569-1802</idno>
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<date when="2014">2014</date>
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<front>
<div type="abstract" xml:lang="en">
<p id="P2">Cardiovascular homeostasis and health is maintained through the balanced interactions of cardiac generated blood flow and cross-talk between the cellular components that comprise blood vessels. Central to this cross-talk is endothelial generated nitric oxide (NO) that stimulates relaxation of the contractile vascular smooth muscle (VSMC) layer of blood vessels. In cardiovascular disease this balanced interaction is disrupted and NO signaling lost. Work over the last several years indicates regulation of NO is much more complex than previously believed. It is now apparent the secreted protein thrombospondin-1 (TSP1), that is upregulated in cardiovascular disease and animal models of the same, on activating cell surface receptor CD47, redundantly inhibits NO production and NO signaling. This inhibitory event has implications for baseline and disease-related responses mediated by NO. Further work has identified that TSP1-CD47 signaling stimulates enzymatic reactive oxygen species (ROS) production to further limit blood flow and promote vascular disease. Herein consideration is given to the most recent discoveries in this regard which identify the TSP1-CD47 axis as a major proximate governor of cardiovascular health.</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>
<pmc-dir>properties manuscript</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-journal-id">9432592</journal-id>
<journal-id journal-id-type="pubmed-jr-id">8496</journal-id>
<journal-id journal-id-type="nlm-ta">Matrix Biol</journal-id>
<journal-id journal-id-type="iso-abbrev">Matrix Biol.</journal-id>
<journal-title-group>
<journal-title>Matrix biology : journal of the International Society for Matrix Biology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0945-053X</issn>
<issn pub-type="epub">1569-1802</issn>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">24418252</article-id>
<article-id pub-id-type="pmc">4096433</article-id>
<article-id pub-id-type="doi">10.1016/j.matbio.2014.01.002</article-id>
<article-id pub-id-type="manuscript">NIHMS555606</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Thrombospondin-1 and CD47 Regulation of Cardiac, Pulmonary and Vascular Responses in Health and Disease</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Rogers</surname>
<given-names>Natasha M.</given-names>
</name>
<degrees>MD, PhD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Sharifi-Sanjani</surname>
<given-names>Maryam</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Csányi</surname>
<given-names>Gábor</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Pagano</surname>
<given-names>Patrick J.</given-names>
</name>
<degrees>PhD</degrees>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Isenberg</surname>
<given-names>Jeffrey S.</given-names>
</name>
<degrees>MD, MPH</degrees>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="aff" rid="A3">3</xref>
<xref ref-type="aff" rid="A4">4</xref>
<xref rid="FN1" ref-type="author-notes">§</xref>
</contrib>
</contrib-group>
<aff id="A1">
<label>1</label>
Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</aff>
<aff id="A2">
<label>2</label>
Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</aff>
<aff id="A3">
<label>3</label>
Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</aff>
<aff id="A4">
<label>4</label>
Starzl Transplantation Institute, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261</aff>
<author-notes>
<corresp id="FN1">
<label>§</label>
To whom correspondence may be addressed: Jeffrey S. Isenberg, MD, MPH, BST, Room E1258, 200 Lothrop Street, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, Phone: (412) 383-5424,
<email>jsi5@pitt.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted">
<day>19</day>
<month>2</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub">
<day>11</day>
<month>1</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="ppub">
<month>7</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>01</day>
<month>7</month>
<year>2015</year>
</pub-date>
<volume>0</volume>
<fpage>92</fpage>
<lpage>101</lpage>
<pmc-comment>elocation-id from pubmed: 10.1016/j.matbio.2014.01.002</pmc-comment>
<permissions>
<copyright-statement>© 2014 The Authors. Published by Elsevier B.V. and International Society of Matrix Biology. All rights reserved.</copyright-statement>
<copyright-year>2014</copyright-year>
</permissions>
<abstract>
<p id="P2">Cardiovascular homeostasis and health is maintained through the balanced interactions of cardiac generated blood flow and cross-talk between the cellular components that comprise blood vessels. Central to this cross-talk is endothelial generated nitric oxide (NO) that stimulates relaxation of the contractile vascular smooth muscle (VSMC) layer of blood vessels. In cardiovascular disease this balanced interaction is disrupted and NO signaling lost. Work over the last several years indicates regulation of NO is much more complex than previously believed. It is now apparent the secreted protein thrombospondin-1 (TSP1), that is upregulated in cardiovascular disease and animal models of the same, on activating cell surface receptor CD47, redundantly inhibits NO production and NO signaling. This inhibitory event has implications for baseline and disease-related responses mediated by NO. Further work has identified that TSP1-CD47 signaling stimulates enzymatic reactive oxygen species (ROS) production to further limit blood flow and promote vascular disease. Herein consideration is given to the most recent discoveries in this regard which identify the TSP1-CD47 axis as a major proximate governor of cardiovascular health.</p>
</abstract>
<kwd-group>
<kwd>Thrombospondin-1</kwd>
<kwd>CD47</kwd>
<kwd>nitric oxide</kwd>
<kwd>blood flow</kwd>
<kwd>cardiovascular disease</kwd>
<kwd>ROS</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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