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Título
Circulating soluble endoglin modifies the inflammatory response in mice
Autor(es)
Palabras clave
Inflammation
Inflammatory diseases
Cardiovascular diseases
Clasificación UNESCO
3209 Farmacología
Fecha de publicación
2017
Editor
Public Library of Science (New York)
Citación
Ruiz-Remolina L, Ollauri-Ibáñez C, Pérez-Roque L, Núñez-Gómez E, Pérez-Barriocanal F, López-Novoa JM, et al. (2017) Circulating soluble endoglin modifies the inflammatory response in mice. PLoS ONE 12(11): e0188204
Resumen
[EN]Inflammation is associated with every health condition, and is an important component of
many pathologies such as cardiovascular diseases. Circulating levels of soluble endoglin
have been shown to be higher in the serum of patients with cardiovascular diseases with a
significant inflammatory component. The aim of this study was to evaluate the implication of
circulating soluble endoglin in the inflammatory response. For this purpose, a transgenic
mouse expressing human soluble endoglin (sEng+) was employed, and three different
inflammatory approaches were used to mimic inflammatory conditions in different tissues.
This study shows that control sEng+ mice have a normal inflammatory state. The lung and
kidney injury induced by the inflammatory agents was reduced in sEng+ mice, especially
the intra-alveolar and kidney infiltrates, suggesting a possible reduction in inflammation
induced by soluble endoglin. To deepen into this possible effect, the leukocyte number in
the bronchoalveolar lavage and air pouch lavage was evaluated and a significant reduction
of neutrophil infiltration in LPS-treated lungs and ischemic kidneys from sEng+ with respect
to WT mice was observed. Additionally, the mechanisms through which soluble endoglin
prevents inflammation were studied. We found that in sEng+ animals the increment of
proinflammatory cytokines, TNFα, IL1β and IL6, induced by the inflammatory stimulus
was reduced. Soluble endoglin also prevents the augmented adhesion molecules, ICAM,
VCAM and E-selectin induced by the inflammatory stimulus. In addition, vascular permeability
increased by inflammatory agents was also reduced by soluble endoglin. These results
suggest that soluble endoglin modulates inflammatory-related diseases and open new perspectives
leading to the development of novel and targeted approaches for the prevention
and treatment of cardiovascular diseases.
URI
ISSN
1932-6203
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