Esperanza Alonso
University of Valladolid
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Publication
Featured researches published by Esperanza Alonso.
Pflügers Archiv: European Journal of Physiology | 2015
Pilar Cidad; Eduardo Miguel-Velado; Christian Ruiz-McDavitt; Esperanza Alonso; Laura Jiménez-Pérez; Agustín Asuaje; Yamila Carmona; Daniel García-Arribas; Javier López; Yngrid Marroquín; Mirella Fernández; Mercè Roqué; M. Teresa Pérez-García; José R. López-López
Phenotypic modulation (PM) of vascular smooth muscle cells (VSMCs) is central to the process of intimal hyperplasia which constitutes a common pathological lesion in occlusive vascular diseases. Changes in the functional expression of Kv1.5 and Kv1.3 currents upon PM in mice VSMCs have been found to contribute to cell migration and proliferation. Using human VSMCs from vessels in which unwanted remodeling is a relevant clinical complication, we explored the contribution of the Kv1.5 to Kv1.3 switch to PM. Changes in the expression and the functional contribution of Kv1.3 and Kv1.5 channels were studied in contractile and proliferating VSMCs obtained from human donors. Both a Kv1.5 to Kv1.3 switch upon PM and an anti-proliferative effect of Kv1.3 blockers on PDGF-induced proliferation were observed in all vascular beds studied. When investigating the signaling pathways modulated by the blockade of Kv1.3 channels, we found that anti-proliferative effects of Kv1.3 blockers on human coronary artery VSMCs were occluded by selective inhibition of MEK/ERK and PLCγ signaling pathways, but were unaffected upon blockade of PI3K/mTOR pathway. The temporal course of the anti-proliferative effects of Kv1.3 blockers indicates that they have a role in the late signaling events essential for the mitogenic response to growth factors. These findings establish the involvement of Kv1.3 channels in the PM of human VSMCs. Moreover, as current therapies to prevent restenosis rely on mTOR blockers, our results provide the basis for the development of novel, more specific therapies.
Journal of Biological Chemistry | 2016
Laura Jiménez-Pérez; Pilar Cidad; I Alvarez-Miguel; Alba Santos-Hipólito; Rebeca Torres-Merino; Esperanza Alonso; Miguel A. de la Fuente; José R. López-López; M. Teresa Pérez-García
Changes in voltage-dependent potassium channels (Kv channels) associate to proliferation in many cell types, including transfected HEK293 cells. In this system Kv1.5 overexpression decreases proliferation, whereas Kv1.3 expression increases it independently of K+ fluxes. To identify Kv1.3 domains involved in a proliferation-associated signaling mechanism(s), we constructed chimeric Kv1.3-Kv1.5 channels and point-mutant Kv1.3 channels, which were expressed as GFP- or cherry-fusion proteins. We studied their trafficking and functional expression, combining immunocytochemical and electrophysiological methods, and their impact on cell proliferation. We found that the C terminus is necessary for Kv1.3-induced proliferation. We distinguished two residues (Tyr-447 and Ser-459) whose mutation to alanine abolished proliferation. The insertion into Kv1.5 of a sequence comprising these two residues increased proliferation rate. Moreover, Kv1.3 voltage-dependent transitions from closed to open conformation induced MEK-ERK1/2-dependent Tyr-447 phosphorylation. We conclude that the mechanisms for Kv1.3-induced proliferation involve the accessibility of key docking sites at the C terminus. For one of these sites (Tyr-447) we demonstrated the contribution of MEK/ERK-dependent phosphorylation, which is regulated by voltage-induced conformational changes.
Journal of the American College of Cardiology | 2015
Mercè Roqué; Manel Garabito; Solanes Nuria; Montserrat Rigol; Pilar Cidad; M. Teresa Pérez-García; Victor Ramos; José Ramón López; Salvador Borrós; Esperanza Alonso; Laura Jimenez Perez
Vascular smooth muscle cells (VSMCs) switch from a contractile to a proliferative phenotype, in response to arterial injury, such as after percutaneous coronary interventions (PCI). This phenotypic switch implies a profound change in the expression of contractile proteins and ion channels. In a
Archive | 2004
Rocío Díaz; Esperanza Alonso; J Fernandez Lopez
Space Science Reviews | 2018
Leo Metcalfe; M. Aberasturi; Esperanza Alonso; Rosa Alvarez; Mike Ashman; Isa Barbarisi; J. Brumfitt; A. Cardesín; D. Coia; Marc Costa; Ramos Fernández; D. J. Frew; J. Gallegos; J. J. García Beteta; Bernhard Geiger; D. Heather; T. Lim; Patricia Martín; C. Muñoz Crego; M. Muñoz Fernandez; A. Villacorta
Biophysical Journal | 2018
M. Teresa Pérez-García; Pilar Cidad; Esperanza Alonso; Pablo Fernández-Velasco; Miguel A. de la Fuente; José R. López-López
Biophysical Journal | 2016
Teresa Pérez-García; Pilar Cidad; Laura Jiménez-Pérez; I Alvarez-Miguel; Alba Santos-Hipólito; Esperanza Alonso; Miguel A. de la Fuente; José R. López-López
Proceedings of The Physiological Society | 2014
Laura Jiménez-Pérez; Pilar Cidad; I Alvarez-Miguel; R Torres-Merino; Esperanza Alonso; Ma de la Fuente; Jr L; M Perez-Garcia
Proceedings of The Physiological Society | 2014
I Alvarez-Miguel; Pilar Cidad; Esperanza Alonso; M Perez-Garcia; Jr L
Journal of the American College of Cardiology | 2012
Mercè Roquè. Laura Novensa; Pilar Cidad; Montserrat Batlle; Eduardo Miguel-Velado; Esperanza Alonso; Teresa Pérez-García; José Ramón López; Magda Heras