Lymphangiogenesis in myocardial remodelling after infarction
Identifieur interne : 003B35 ( Pmc/Checkpoint ); précédent : 003B34; suivant : 003B36Lymphangiogenesis in myocardial remodelling after infarction
Auteurs : Y. Ishikawa ; Y. Akishima-Fukasawa ; K. Ito ; Y. Akasaka ; M. Tanaka ; R. Shimokawa ; M. Kimura-Matsumoto ; H. Morita ; S. Sato ; I. Kamata ; T. IshiiSource :
- Histopathology [ 0309-0167 ] ; 2007.
Abstract
Ishikawa Y, Akishima-Fukasawa Y, Ito K, Akasaka Y, Tanaka M, Shimokawa R, Kimura-Matsumoto M, Morita H, Sato S, Kamata I & Ishii T (2007)
The lymphatic system is involved in fluid homeostasis of the cardiac interstitium, but lymphangiogenesis in myocardial remodelling has not previously been examined histopathologically. The aim was to investigate by D2-40 immunohistochemistry the sequential changes in lymphatic distribution in the process of myocardial remodelling after myocardial infarction (MI).
Myocardial tissues in various phases of healing after MI were obtained from 40 autopsied hearts. D2-40+ lymphatic vessel density (LD) and CD34+ blood vessel density (BD) in the lesion were determined. BD decreased with advance of myocardial necrosis, subsequently increased at the early stage of granulation and thereafter decreased with the progression of scar formation. In contrast, lymphatic vessels were not detected in lesions with coagulation necrosis, and newly formed lymphatics first appeared in the early stages of granulation. A subsequent increase in LD was demonstrated in the late stages of granulation, and lymphatics remained up to the scar phase. Vascular endothelial growth factor-C was consistently expressed in viable cardiomyocytes around the lesion in all of these stages.
In myocardial remodelling after MI, lymphangiogenesis lags behind blood vessel angiogenesis; newly formed lymphatics may be involved mainly in the maturation of fibrosis and scar formation through the drainage of excessive proteins and fluid.
Url:
DOI: 10.1111/j.1365-2559.2007.02785.x
PubMed: 17727476
PubMed Central: 2366023
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Shimokawa</name></author><author><name sortKey="Kimura Matsumoto, M" sort="Kimura Matsumoto, M" uniqKey="Kimura Matsumoto M" first="M" last="Kimura-Matsumoto">M. Kimura-Matsumoto</name></author><author><name sortKey="Morita, H" sort="Morita, H" uniqKey="Morita H" first="H" last="Morita">H. Morita</name></author><author><name sortKey="Sato, S" sort="Sato, S" uniqKey="Sato S" first="S" last="Sato">S. Sato</name></author><author><name sortKey="Kamata, I" sort="Kamata, I" uniqKey="Kamata I" first="I" last="Kamata">I. Kamata</name></author><author><name sortKey="Ishii, T" sort="Ishii, T" uniqKey="Ishii T" first="T" last="Ishii">T. 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Ishikawa</name></author><author><name sortKey="Akishima Fukasawa, Y" sort="Akishima Fukasawa, Y" uniqKey="Akishima Fukasawa Y" first="Y" last="Akishima-Fukasawa">Y. Akishima-Fukasawa</name></author><author><name sortKey="Ito, K" sort="Ito, K" uniqKey="Ito K" first="K" last="Ito">K. Ito</name></author><author><name sortKey="Akasaka, Y" sort="Akasaka, Y" uniqKey="Akasaka Y" first="Y" last="Akasaka">Y. Akasaka</name></author><author><name sortKey="Tanaka, M" sort="Tanaka, M" uniqKey="Tanaka M" first="M" last="Tanaka">M. Tanaka</name></author><author><name sortKey="Shimokawa, R" sort="Shimokawa, R" uniqKey="Shimokawa R" first="R" last="Shimokawa">R. Shimokawa</name></author><author><name sortKey="Kimura Matsumoto, M" sort="Kimura Matsumoto, M" uniqKey="Kimura Matsumoto M" first="M" last="Kimura-Matsumoto">M. Kimura-Matsumoto</name></author><author><name sortKey="Morita, H" sort="Morita, H" uniqKey="Morita H" first="H" last="Morita">H. Morita</name></author><author><name sortKey="Sato, S" sort="Sato, S" uniqKey="Sato S" first="S" last="Sato">S. Sato</name></author><author><name sortKey="Kamata, I" sort="Kamata, I" uniqKey="Kamata I" first="I" last="Kamata">I. Kamata</name></author><author><name sortKey="Ishii, T" sort="Ishii, T" uniqKey="Ishii T" first="T" last="Ishii">T. Ishii</name></author></analytic><series><title level="j">Histopathology</title><idno type="ISSN">0309-0167</idno><idno type="eISSN">1365-2559</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Ishikawa Y, Akishima-Fukasawa Y, Ito K, Akasaka Y, Tanaka M, Shimokawa R, Kimura-Matsumoto M, Morita H, Sato S, Kamata I & Ishii T (2007) <italic>Histopathology</italic><bold>51,</bold> 345–353</p><p><bold>Lymphangiogenesis in myocardial remodelling after infarction</bold></p><sec><title>Aims</title><p>The lymphatic system is involved in fluid homeostasis of the cardiac interstitium, but lymphangiogenesis in myocardial remodelling has not previously been examined histopathologically. The aim was to investigate by D2-40 immunohistochemistry the sequential changes in lymphatic distribution in the process of myocardial remodelling after myocardial infarction (MI).</p></sec><sec sec-type="methods"><title>Methods and results</title><p>Myocardial tissues in various phases of healing after MI were obtained from 40 autopsied hearts. D2-40+ lymphatic vessel density (LD) and CD34+ blood vessel density (BD) in the lesion were determined. BD decreased with advance of myocardial necrosis, subsequently increased at the early stage of granulation and thereafter decreased with the progression of scar formation. In contrast, lymphatic vessels were not detected in lesions with coagulation necrosis, and newly formed lymphatics first appeared in the early stages of granulation. A subsequent increase in LD was demonstrated in the late stages of granulation, and lymphatics remained up to the scar phase. Vascular endothelial growth factor-C was consistently expressed in viable cardiomyocytes around the lesion in all of these stages.</p></sec><sec><title>Conclusion</title><p>In myocardial remodelling after MI, lymphangiogenesis lags behind blood vessel angiogenesis; newly formed lymphatics may be involved mainly in the maturation of fibrosis and scar formation through the drainage of excessive proteins and fluid.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Histopathology</journal-id><journal-id journal-id-type="publisher-id">his</journal-id><journal-title>Histopathology</journal-title><issn pub-type="ppub">0309-0167</issn><issn pub-type="epub">1365-2559</issn><publisher><publisher-name>Blackwell Publishing Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">17727476</article-id><article-id pub-id-type="pmc">2366023</article-id><article-id pub-id-type="doi">10.1111/j.1365-2559.2007.02785.x</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Articles</subject></subj-group></article-categories><title-group><article-title>Lymphangiogenesis in myocardial remodelling after infarction</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ishikawa</surname><given-names>Y</given-names></name></contrib><contrib contrib-type="author"><name><surname>Akishima-Fukasawa</surname><given-names>Y</given-names></name><xref ref-type="aff" rid="au1">1</xref></contrib><contrib contrib-type="author"><name><surname>Ito</surname><given-names>K</given-names></name></contrib><contrib contrib-type="author"><name><surname>Akasaka</surname><given-names>Y</given-names></name></contrib><contrib contrib-type="author"><name><surname>Tanaka</surname><given-names>M</given-names></name><xref ref-type="aff" rid="au2">2</xref></contrib><contrib contrib-type="author"><name><surname>Shimokawa</surname><given-names>R</given-names></name><xref ref-type="aff" rid="au3">3</xref></contrib><contrib contrib-type="author"><name><surname>Kimura-Matsumoto</surname><given-names>M</given-names></name></contrib><contrib contrib-type="author"><name><surname>Morita</surname><given-names>H</given-names></name><xref ref-type="aff" rid="au4">4</xref></contrib><contrib contrib-type="author"><name><surname>Sato</surname><given-names>S</given-names></name><xref ref-type="aff" rid="au4">4</xref></contrib><contrib contrib-type="author"><name><surname>Kamata</surname><given-names>I</given-names></name><xref ref-type="aff" rid="au4">4</xref></contrib><contrib contrib-type="author"><name><surname>Ishii</surname><given-names>T</given-names></name></contrib><aff><institution>Department of Pathology, Toho University School of Medicine</institution><addr-line>Tokyo, Japan</addr-line></aff><aff id="au1"><label>1</label><institution>Pathology Division, National Cancer Centre Research Institute</institution><addr-line>Tokyo, Japan</addr-line></aff><aff id="au2"><label>2</label><institution>Pathology Division, Tokyo Metropolitan Hiroo Hospital</institution><addr-line>Tokyo, Japan</addr-line></aff><aff id="au3"><label>3</label><institution>Pathology Division, Omori Red Cross Hospital</institution><addr-line>Tokyo, Japan</addr-line></aff><aff id="au4"><label>4</label><institution>Department of Gastroenterology and Hepatology, Toho University Medical Centre Omori Hospital</institution><addr-line>Tokyo, Japan</addr-line></aff></contrib-group><author-notes><corresp id="cor1">Address for correspondence: Yukio Ishikawa, MD, Department of Pathology, Toho University School of Medicine, 5-21-16 Omori-nishi, Ohta-ku, Tokyo 143-8540, Japan. e-mail: <email>yukio@med.toho-u.ac.jp</email></corresp><fn><p>Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.</p></fn></author-notes><pub-date pub-type="ppub"><day>01</day><month>9</month><year>2007</year></pub-date><volume>51</volume><issue>3</issue><fpage>345</fpage><lpage>353</lpage><history><date date-type="received"><day>21</day><month>9</month><year>2006</year></date><date date-type="accepted"><day>01</day><month>3</month><year>2007</year></date></history><copyright-statement>© 2007 The Authors. Journal compilation 2007 Blackwell Publishing Limited.</copyright-statement><copyright-year>2007</copyright-year><abstract><p>Ishikawa Y, Akishima-Fukasawa Y, Ito K, Akasaka Y, Tanaka M, Shimokawa R, Kimura-Matsumoto M, Morita H, Sato S, Kamata I & Ishii T (2007) <italic>Histopathology</italic><bold>51,</bold> 345–353</p><p><bold>Lymphangiogenesis in myocardial remodelling after infarction</bold></p><sec><title>Aims</title><p>The lymphatic system is involved in fluid homeostasis of the cardiac interstitium, but lymphangiogenesis in myocardial remodelling has not previously been examined histopathologically. The aim was to investigate by D2-40 immunohistochemistry the sequential changes in lymphatic distribution in the process of myocardial remodelling after myocardial infarction (MI).</p></sec><sec sec-type="methods"><title>Methods and results</title><p>Myocardial tissues in various phases of healing after MI were obtained from 40 autopsied hearts. D2-40+ lymphatic vessel density (LD) and CD34+ blood vessel density (BD) in the lesion were determined. BD decreased with advance of myocardial necrosis, subsequently increased at the early stage of granulation and thereafter decreased with the progression of scar formation. In contrast, lymphatic vessels were not detected in lesions with coagulation necrosis, and newly formed lymphatics first appeared in the early stages of granulation. A subsequent increase in LD was demonstrated in the late stages of granulation, and lymphatics remained up to the scar phase. Vascular endothelial growth factor-C was consistently expressed in viable cardiomyocytes around the lesion in all of these stages.</p></sec><sec><title>Conclusion</title><p>In myocardial remodelling after MI, lymphangiogenesis lags behind blood vessel angiogenesis; newly formed lymphatics may be involved mainly in the maturation of fibrosis and scar formation through the drainage of excessive proteins and fluid.</p></sec></abstract><kwd-group><kwd>blood vessel</kwd><kwd>lymphangiogenesis</kwd><kwd>lymphatic vessel</kwd><kwd>myocardial infarction</kwd><kwd>myocardial remodelling</kwd><kwd>vascular endothelial growth factor-C</kwd></kwd-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Akasaka, Y" sort="Akasaka, Y" uniqKey="Akasaka Y" first="Y" last="Akasaka">Y. Akasaka</name><name sortKey="Akishima Fukasawa, Y" sort="Akishima Fukasawa, Y" uniqKey="Akishima Fukasawa Y" first="Y" last="Akishima-Fukasawa">Y. Akishima-Fukasawa</name><name sortKey="Ishii, T" sort="Ishii, T" uniqKey="Ishii T" first="T" last="Ishii">T. Ishii</name><name sortKey="Ishikawa, Y" sort="Ishikawa, Y" uniqKey="Ishikawa Y" first="Y" last="Ishikawa">Y. Ishikawa</name><name sortKey="Ito, K" sort="Ito, K" uniqKey="Ito K" first="K" last="Ito">K. Ito</name><name sortKey="Kamata, I" sort="Kamata, I" uniqKey="Kamata I" first="I" last="Kamata">I. Kamata</name><name sortKey="Kimura Matsumoto, M" sort="Kimura Matsumoto, M" uniqKey="Kimura Matsumoto M" first="M" last="Kimura-Matsumoto">M. Kimura-Matsumoto</name><name sortKey="Morita, H" sort="Morita, H" uniqKey="Morita H" first="H" last="Morita">H. Morita</name><name sortKey="Sato, S" sort="Sato, S" uniqKey="Sato S" first="S" last="Sato">S. Sato</name><name sortKey="Shimokawa, R" sort="Shimokawa, R" uniqKey="Shimokawa R" first="R" last="Shimokawa">R. Shimokawa</name><name sortKey="Tanaka, M" sort="Tanaka, M" uniqKey="Tanaka M" first="M" last="Tanaka">M. Tanaka</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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