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Título

S-endoglin expression is induced in senescent endothelial cells and contributes to vascular pathology

AutorBlanco, Francisco J. ; Grande, Maria T.; Langa, Carmen ; Oujo, Barbara; Velasco, Soraya; Rodríguez-Barbero, Alicia; Pérez-Gómez, Eduardo ; Quintanilla, Miguel ; Lopez-Novoa, José Miguel; Bernabéu, Carmelo
Palabras claveAging
TGF-β receptors
Fecha de publicación5-dic-2008
EditorAmerican Heart Association
CitaciónCirculation Research 103(12): 1383-1392 (2008)
ResumenSenescence of endothelial cells (ECs) may contribute to age-associated cardiovascular diseases, including atherosclerosis and hypertension. The functional and gene expression changes associated with cellular senescence are poorly understood. Here, we have analyzed the expression, during EC senescence, of 2 different isoforms (L, long; S, short) of endoglin, an auxiliary transforming growth factor (TGF)-beta receptor involved in vascular remodeling and angiogenesis. As evidenced by RT-PCR, the S/L ratio of endoglin isoforms was increased during senescence of human ECs in vitro, as well as during aging of mice in vascularized tissues. Next, the effect of S-endoglin protein on the TGF-beta receptor complex was studied. As revealed by coimmunoprecipitation assays, S-endoglin was able to interact with both TGF-beta type I receptors, ALK5 and ALK1, although the interaction with ALK5 was stronger than with ALK1. S-endoglin conferred a lower proliferation rate to ECs and behaved differently from L-endoglin in relation to TGF-beta-responsive reporters with ALK1 or ALK5 specificities, mimicking the behavior of the endothelial senescence markers Id1 and plasminogen activator inhibitor-1. In situ hybridization studies demonstrated the expression of S-endoglin in the endothelium from human arteries. Transgenic mice overexpressing S-endoglin in ECs showed hypertension, decreased hypertensive response to NO inhibition, decreased vasodilatory response to TGF-beta(1) administration, and decreased endothelial nitric oxide synthase expression in lungs and kidneys, supporting the involvement of S-endoglin in the NO-dependent vascular homeostasis. Taken together, these results suggest that S-endoglin is induced during endothelial senescence and may contribute to age-dependent vascular pathology.
Versión del editorhttp://dx.doi.org/10.1161/CIRCRESAHA.108.176552
URIhttp://hdl.handle.net/10261/21814
DOI10.1161/CIRCRESAHA.108.176552
ISSN0009-7330
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