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Angiopoietin-2 in experimental colitis

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Angiopoietin-2 in experimental colitis

Auteurs : Vijay C. Ganta [États-Unis] ; Walter Cromer [États-Unis] ; Ginny L. Mills [États-Unis] ; James Traylor [États-Unis] ; Merilyn Jennings [États-Unis] ; Sarah Daley [États-Unis] ; Benjamin Clark [États-Unis] ; J. Michael Mathis [États-Unis] ; Michael Bernas [États-Unis] ; Paul Jordan [États-Unis] ; Marlys Witte [États-Unis] ; J. Steven Alexander [États-Unis]

Source :

Inflammatory bowel diseases [ 1078-0998 ] ; 2010.

RBID : PMC:2881632

Abstract

The pathophysiology of inflammatory bowel disease (IBD) includes leukocyte infiltration, blood and lymphatic remodeling, weight loss and protein enteropathy. The roles of angiopoietin-2 (Ang-2) in initiating gut inflammation, leukocyte infiltration and angiogenesis are not well understood. Several important differences were seen in the development of experimental IBD in Ang-2^-/- mice. Although weight change and disease activity differ only slightly in WT and Ang-2^-/- + DSS treated mice, leukocyte infiltration, inflammation and blood and lymphatic vessel density is significantly attenuated compared to WT+ DSS mice. Gut capillary fragility and water export (stool blood and form) appear significantly earlier in Ang-2^-/- + DSS mice vs. WT. Colon lengths were also significantly reduced in Ang-2^-/- and gut histopathology was less severe in Ang-2^-/-compared to WT + DSS. Lastly, the decrease in serum protein content in WT + DSS was less severe in Ang-2^-/- + DSS, thus protein losing enteropathy (PLE) a feature of IBD is relieved by Ang-2^-/-. These data demonstrate that in DSS colitis, Ang-2 mediates inflammatory hemangiogenesis, lymphangiogenesis and neutrophil infiltration to reduce some, but not all clinical features of IBD. The implications for Ang-2 manipulation in the development of IBD and other inflammatory diseases and treatments involving Ang-2 are discussed.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881632

DOI: 10.1002/ibd.21150
PubMed: 19902545
PubMed Central: 2881632

Affiliations:

Le document en format XML

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<affiliation wicri:level="2"><nlm:aff id="A2">Department of Cell Biology and Anatomy Louisiana Health Sciences Centre-Shreveport, Louisiana</nlm:aff>
<country xml:lang="fr">États-Unis</country>
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<country xml:lang="fr">États-Unis</country>
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<series><title level="j">Inflammatory bowel diseases</title>
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<front><div type="abstract" xml:lang="en"><p id="P1">The pathophysiology of inflammatory bowel disease (IBD) includes leukocyte infiltration, blood and lymphatic remodeling, weight loss and protein enteropathy. The roles of angiopoietin-2 (Ang-2) in initiating gut inflammation, leukocyte infiltration and angiogenesis are not well understood. Several important differences were seen in the development of experimental IBD in Ang-2<sup>-/-</sup>
 mice. Although weight change and disease activity differ only slightly in WT and Ang-2<sup>-/-</sup>
 + DSS treated mice, leukocyte infiltration, inflammation and blood and lymphatic vessel density is significantly attenuated compared to WT+ DSS mice. Gut capillary fragility and water export (stool blood and form) appear significantly earlier in Ang-2<sup>-/-</sup>
 + DSS mice vs. WT. Colon lengths were also significantly reduced in Ang-2<sup>-/-</sup>
 and gut histopathology was less severe in Ang-2<sup>-/-</sup>
compared to WT + DSS. Lastly, the decrease in serum protein content in WT + DSS was less severe in Ang-2<sup>-/-</sup>
 + DSS, thus protein losing enteropathy (PLE) a feature of IBD is relieved by Ang-2<sup>-/-</sup>
. These data demonstrate that in DSS colitis, Ang-2 mediates inflammatory hemangiogenesis, lymphangiogenesis and neutrophil infiltration to reduce some, but not all clinical features of IBD. The implications for Ang-2 manipulation in the development of IBD and other inflammatory diseases and treatments involving Ang-2 are discussed.</p>
</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
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<region><li>Arizona</li>
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<tree><country name="États-Unis"><region name="Louisiane"><name sortKey="Ganta, Vijay C" sort="Ganta, Vijay C" uniqKey="Ganta V" first="Vijay C." last="Ganta">Vijay C. Ganta</name>
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<name sortKey="Bernas, Michael" sort="Bernas, Michael" uniqKey="Bernas M" first="Michael" last="Bernas">Michael Bernas</name>
<name sortKey="Clark, Benjamin" sort="Clark, Benjamin" uniqKey="Clark B" first="Benjamin" last="Clark">Benjamin Clark</name>
<name sortKey="Cromer, Walter" sort="Cromer, Walter" uniqKey="Cromer W" first="Walter" last="Cromer">Walter Cromer</name>
<name sortKey="Daley, Sarah" sort="Daley, Sarah" uniqKey="Daley S" first="Sarah" last="Daley">Sarah Daley</name>
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<name sortKey="Jordan, Paul" sort="Jordan, Paul" uniqKey="Jordan P" first="Paul" last="Jordan">Paul Jordan</name>
<name sortKey="Michael Mathis, J" sort="Michael Mathis, J" uniqKey="Michael Mathis J" first="J." last="Michael Mathis">J. Michael Mathis</name>
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<name sortKey="Steven Alexander, J" sort="Steven Alexander, J" uniqKey="Steven Alexander J" first="J." last="Steven Alexander">J. Steven Alexander</name>
<name sortKey="Traylor, James" sort="Traylor, James" uniqKey="Traylor J" first="James" last="Traylor">James Traylor</name>
<name sortKey="Witte, Marlys" sort="Witte, Marlys" uniqKey="Witte M" first="Marlys" last="Witte">Marlys Witte</name>
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Serveur d'exploration sur le lymphœdème

Angiopoietin-2 in experimental colitis

Angiopoietin-2 in experimental colitis

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Abstract

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