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<dc:creator>Ruiz Remolina, Laura</dc:creator>
<dc:creator>Ollauri Ibáñez, Claudia</dc:creator>
<dc:creator>Pérez Roque, Lucía</dc:creator>
<dc:creator>Núñez Gómez, Elena</dc:creator>
<dc:creator>Pérez Barriocanal, Fernando</dc:creator>
<dc:creator>López-Novoa, José M.</dc:creator>
<dc:creator>Pericacho Bustos, Miguel</dc:creator>
<dc:creator>Rodríguez Barbero, Alicia</dc:creator>
<dc:date>2017</dc:date>
<dc:description>[EN]Inflammation is associated with every health condition, and is an important component of&#xd;
many pathologies such as cardiovascular diseases. Circulating levels of soluble endoglin&#xd;
have been shown to be higher in the serum of patients with cardiovascular diseases with a&#xd;
significant inflammatory component. The aim of this study was to evaluate the implication of&#xd;
circulating soluble endoglin in the inflammatory response. For this purpose, a transgenic&#xd;
mouse expressing human soluble endoglin (sEng+) was employed, and three different&#xd;
inflammatory approaches were used to mimic inflammatory conditions in different tissues.&#xd;
This study shows that control sEng+ mice have a normal inflammatory state. The lung and&#xd;
kidney injury induced by the inflammatory agents was reduced in sEng+ mice, especially&#xd;
the intra-alveolar and kidney infiltrates, suggesting a possible reduction in inflammation&#xd;
induced by soluble endoglin. To deepen into this possible effect, the leukocyte number in&#xd;
the bronchoalveolar lavage and air pouch lavage was evaluated and a significant reduction&#xd;
of neutrophil infiltration in LPS-treated lungs and ischemic kidneys from sEng+ with respect&#xd;
to WT mice was observed. Additionally, the mechanisms through which soluble endoglin&#xd;
prevents inflammation were studied. We found that in sEng+ animals the increment of&#xd;
proinflammatory cytokines, TNFα, IL1β and IL6, induced by the inflammatory stimulus&#xd;
was reduced. Soluble endoglin also prevents the augmented adhesion molecules, ICAM,&#xd;
VCAM and E-selectin induced by the inflammatory stimulus. In addition, vascular permeability&#xd;
increased by inflammatory agents was also reduced by soluble endoglin. These results&#xd;
suggest that soluble endoglin modulates inflammatory-related diseases and open new perspectives&#xd;
leading to the development of novel and targeted approaches for the prevention&#xd;
and treatment of cardiovascular diseases.</dc:description>
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<dc:identifier>http://hdl.handle.net/10366/135817</dc:identifier>
<dc:language>eng</dc:language>
<dc:publisher>Public Library of Science (New York)</dc:publisher>
<dc:subject>3209 Farmacología</dc:subject>
<dc:title>Circulating soluble endoglin modifies the inflammatory response in mice</dc:title>
<dc:type>info:eu-repo/semantics/article</dc:type>
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