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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Increased Hyaluronan Expression at Distinct Time Points in Acute Lymphedema</title><author><name sortKey="Roberts, Melissa A" sort="Roberts, Melissa A" uniqKey="Roberts M" first="Melissa A." last="Roberts">Melissa A. Roberts</name></author><author><name sortKey="Mendez, Uziel" sort="Mendez, Uziel" uniqKey="Mendez U" first="Uziel" last="Mendez">Uziel Mendez</name></author><author><name sortKey="Gilbert, Ryan J" sort="Gilbert, Ryan J" uniqKey="Gilbert R" first="Ryan J." last="Gilbert">Ryan J. Gilbert</name></author><author><name sortKey="Keim, Alexander P" sort="Keim, Alexander P" uniqKey="Keim A" first="Alexander P." last="Keim">Alexander P. Keim</name></author><author><name sortKey="Goldman, Jeremy" sort="Goldman, Jeremy" uniqKey="Goldman J" first="Jeremy" last="Goldman">Jeremy Goldman</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22984909</idno><idno type="pmc">3444763</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444763</idno><idno type="RBID">PMC:3444763</idno><idno type="doi">10.1089/lrb.2012.0001</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">003022</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003022</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Increased Hyaluronan Expression at Distinct Time Points in Acute Lymphedema</title><author><name sortKey="Roberts, Melissa A" sort="Roberts, Melissa A" uniqKey="Roberts M" first="Melissa A." last="Roberts">Melissa A. Roberts</name></author><author><name sortKey="Mendez, Uziel" sort="Mendez, Uziel" uniqKey="Mendez U" first="Uziel" last="Mendez">Uziel Mendez</name></author><author><name sortKey="Gilbert, Ryan J" sort="Gilbert, Ryan J" uniqKey="Gilbert R" first="Ryan J." last="Gilbert">Ryan J. Gilbert</name></author><author><name sortKey="Keim, Alexander P" sort="Keim, Alexander P" uniqKey="Keim A" first="Alexander P." last="Keim">Alexander P. Keim</name></author><author><name sortKey="Goldman, Jeremy" sort="Goldman, Jeremy" uniqKey="Goldman J" first="Jeremy" last="Goldman">Jeremy Goldman</name></author></analytic><series><title level="j">Lymphatic Research and Biology</title><idno type="ISSN">1539-6851</idno><idno type="eISSN">1557-8585</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><title>Abstract</title><p>Lymphatic dysfunction in lymphedema results in chronic accumulation of interstitial fluid and life-long tissue swelling. In the absence of restored lymphatic drainage via adequate lymphangiogenesis, the interstitial environment can remodel in ways that decrease the elevated interstitial stress. Presently, relatively little is known about the glycosaminoglycans (GAGs) that become upregulated in the interstitium during lymphedema. We employed a mouse tail model of acute lymphedema that reproduces important features of the chronic human condition to establish a relationship between hyaluronan (HA) and sulfated GAG concentration with tissue swelling. We found that HA was upregulated by tissue injury at day 5 and became upregulated again by skin swelling (HA content increasing by 27% relative to controls at days 15 and 20). Surprisingly, the second phase of HA expression was associated with the declining phase of the tail skin swelling (tail diameter significantly decreasing by 17% from day 10 peak to day 20), demonstrating that HA is upregulated by tissue swelling and may help to counteract the edema in the mouse tail. This finding was confirmed by intradermal injection of an HA degrading enzyme (hyaluronidase) to the swollen tail, which was found to worsen the tail swelling. Sulfated GAGs, including chondroitin sulfate (CS), were not regulated by tissue swelling. The results demonstrate that HA, but not sulfated GAGs, is upregulated in the interstitium by acute tissue swelling. We speculate that HA expression during lymphedema may be part of a natural adaptive mechanism of the interstitial environment to reduce capillary filtration and increase interstitial fluid outflow following lymphatic obstruction and fluid accumulation.</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">Lymphat Res Biol</journal-id><journal-id journal-id-type="iso-abbrev">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></journal-title-group><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></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">22984909</article-id><article-id pub-id-type="pmc">3444763</article-id><article-id pub-id-type="publisher-id">10.1089/lrb.2012.0001</article-id><article-id pub-id-type="doi">10.1089/lrb.2012.0001</article-id><article-categories><subj-group subj-group-type="heading"><subject>Other Original Articles</subject></subj-group></article-categories><title-group><article-title>Increased Hyaluronan Expression at Distinct Time Points in Acute Lymphedema</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Roberts</surname><given-names>Melissa A.</given-names></name><degrees>M.S.</degrees></contrib><contrib contrib-type="author"><name><surname>Mendez</surname><given-names>Uziel</given-names></name></contrib><contrib contrib-type="author"><name><surname>Gilbert</surname><given-names>Ryan J.</given-names></name><degrees>Ph.D.</degrees></contrib><contrib contrib-type="author"><name><surname>Keim</surname><given-names>Alexander P.</given-names></name></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Goldman</surname><given-names>Jeremy</given-names></name><degrees>Ph.D.</degrees></contrib><aff id="aff1">Biomedical Engineering Department,<institution>Michigan Technological University</institution>, Houghton, Michigan.</aff></contrib-group><author-notes><corresp>Address correspondence to: <italic>Jeremy Goldman, Ph.D., Department of Biomedical Engineering, Michigan Technological University, Houghton, MI, 49931. E-mail:</italic><email xlink:href="mailto:jgoldman@mtu.edu">jgoldman@mtu.edu</email></corresp></author-notes><pub-date pub-type="ppub"><month>9</month><year>2012</year><pmc-comment>string-date: September 2012</pmc-comment>
</pub-date><volume>10</volume><issue>3</issue><fpage>122</fpage><lpage>128</lpage><permissions><copyright-statement>Copyright 2012, Mary Ann Liebert, Inc.</copyright-statement><copyright-year>2012</copyright-year></permissions><self-uri xlink:type="simple" xlink:href="lrb.2012.0001.pdf"></self-uri><abstract><title>Abstract</title><p>Lymphatic dysfunction in lymphedema results in chronic accumulation of interstitial fluid and life-long tissue swelling. In the absence of restored lymphatic drainage via adequate lymphangiogenesis, the interstitial environment can remodel in ways that decrease the elevated interstitial stress. Presently, relatively little is known about the glycosaminoglycans (GAGs) that become upregulated in the interstitium during lymphedema. We employed a mouse tail model of acute lymphedema that reproduces important features of the chronic human condition to establish a relationship between hyaluronan (HA) and sulfated GAG concentration with tissue swelling. We found that HA was upregulated by tissue injury at day 5 and became upregulated again by skin swelling (HA content increasing by 27% relative to controls at days 15 and 20). Surprisingly, the second phase of HA expression was associated with the declining phase of the tail skin swelling (tail diameter significantly decreasing by 17% from day 10 peak to day 20), demonstrating that HA is upregulated by tissue swelling and may help to counteract the edema in the mouse tail. This finding was confirmed by intradermal injection of an HA degrading enzyme (hyaluronidase) to the swollen tail, which was found to worsen the tail swelling. Sulfated GAGs, including chondroitin sulfate (CS), were not regulated by tissue swelling. The results demonstrate that HA, but not sulfated GAGs, is upregulated in the interstitium by acute tissue swelling. We speculate that HA expression during lymphedema may be part of a natural adaptive mechanism of the interstitial environment to reduce capillary filtration and increase interstitial fluid outflow following lymphatic obstruction and fluid accumulation.</p></abstract><counts><fig-count count="6"></fig-count><ref-count count="30"></ref-count><page-count count="7"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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