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dc.contributor.author | Molina-Sánchez, Pedro | |
dc.contributor.author | Campo, Lara del | |
dc.contributor.author | Esteban, Vanesa | |
dc.contributor.author | Rius Leiva, Cristina | |
dc.contributor.author | Chèvre, Raphaël | |
dc.contributor.author | Fuster, José Javier | |
dc.contributor.author | Ferrer, Mercedes | |
dc.contributor.author | Redondo, Juan Miguel | |
dc.contributor.author | Andrés, Vicente | |
dc.date.accessioned | 2018-10-20T08:45:43Z | |
dc.date.available | 2018-10-20T08:45:43Z | |
dc.date.issued | 2018 | |
dc.identifier.citation | Molina-Sánchez, P., Del Campo, L., Esteban, V., Rius, C., Chèvre, R., Fuster, J. J., ... & Andrés, V. (2018). Defective p27 phosphorylation at serine 10 affects vascular reactivity and increases abdominal aortic aneurysm development via Cox-2 activation. Journal of Molecular and Cellular Cardiology, 116, 5-15. DOI:10.1016/j.yjmcc.2018.01.010 | spa |
dc.identifier.issn | 0022-2828 | |
dc.identifier.issn | 1095-8584 | |
dc.identifier.uri | http://hdl.handle.net/11268/7477 | |
dc.description.abstract | Phosphorylation at serine 10 (S10) is the major posttranslational modification of the tumor suppressor p27, and is reduced in both human and mouse atherosclerosis. Moreover, a lack of p27-phospho-S10 in apolipoprotein E-null mice (apoE−/−) leads to increased high-fat diet-induced atherosclerosis associated with endothelial dysfunction and augmented leukocyte recruitment. In this study, we analyzed whether p27-phospho-S10 modulates additional endothelial functions and associated pathologies. Defective p27-phospho-S10 increases COX-2 activity in mouse aortic endothelial cells without affecting other key regulators of vascular reactivity, reduces endothelium-dependent dilation, and increases arterial contractility. Lack of p27-phospho-S10 also elevates aortic COX-2 expression and thromboxane A2 production, increases aortic lumen diameter, and aggravates angiotensin II-induced abdominal aortic aneurysm development in apoE−/− mice. All these abnormal responses linked to defective p27-phospho-S10 are blunted by pharmacological inhibition of COX-2. These results demonstrate that defective p27-phospho-S10 modifies endothelial behavior and promotes aneurysm formation via COX-2 activation. | spa |
dc.description.sponsorship | Sin financiación | spa |
dc.language.iso | eng | spa |
dc.title | Defective p27 phosphorylation at serine 10 affects vascular reactivity and increases abdominal aortic aneurysm development via Cox-2 activation | spa |
dc.type | article | spa |
dc.description.impact | 5.055 JCR (2018) Q1, 29/136 Cardiac & Cardiovascular Systems; Q2, 52/193 Cell biology | spa |
dc.description.impact | 2.089 SJR (2018) Q1, 91/421 Molecular Biology, 37/365 Cardiology and Cardiovascular Medicine | spa |
dc.description.impact | No data IDR 2018 | spa |
dc.identifier.doi | 10.1016/j.yjmcc.2018.01.010 | |
dc.rights.accessRights | closedAccess | spa |
dc.subject.uem | Aneurisma abdominal | spa |
dc.subject.unesco | Enfermedad cardiovascular | spa |
dc.description.filiation | UEM | spa |
dc.peerreviewed | Si | spa |
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