Search

Your search keyword '"Mateos-Cáceres, Petra J."' showing total 25 results
Start Over Author "Mateos-Cáceres, Petra J." Publication Year Range Last 50 years
25 results on '"Mateos-Cáceres, Petra J."'

12. New and Old Mechanisms Associated with Hypertension in the Elderly

Author

Mateos-Cáceres, Petra J., Zamorano-León, Jose J., Rodríguez-Sierra, Pablo, Macaya, Carlos, and López-Farré, Antonio J.

Subjects
Article Subject
Abstract

Hypertension is a widely prevalent and important risk factor for cardiovascular diseases that increase with aging. The hallmark of hypertension in the elderly is increased vascular dysfunction. However, the molecular mechanisms by which increased blood pressure leads to vascular injury and impaired endothelial function are not well defined. In the present paper, we will analyze several mechanisms described in the scientific literature involved in hypertension in the elderly as endothelial dysfunction, increased oxygen delivery to tissues, inflammation, cellular apoptosis, and increased concentration of active metabolites. Also, we will focus on new molecular mechanisms involved in hypertension such as telomeres shortening, progenitor cells, circulating microparticles, and epigenetic factors that have appeared as possible causes of hypertension in the elderly. These molecular mechanisms may elucidate different origin for hypertension in the elderly and provide us with new targets for hypertension treatment.

Published
2012
Full Text
View/download PDF

14. Proteomic changes related to “bewildered” circulating platelets in the acute coronary syndrome

Author

López-Farré, Antonio J., primary, Zamorano-Leon, Jose J., additional, Azcona, Luis, additional, Modrego, Javier, additional, Mateos-Cáceres, Petra J., additional, González-Armengol, Juan, additional, Villarroel, Pedro, additional, Moreno-Herrero, Rosario, additional, Rodríguez-Sierra, Pablo, additional, Segura, Antonio, additional, Tamargo, Juan, additional, and Macaya, Carlos, additional

Published
2011
Full Text
View/download PDF

17. Effect of parathyroid-hormone-related protein on human platelet activation

Author

Ortega, Arantxa, primary, Pérez de Prada, Ma Teresa, additional, Mateos-Cáceres, Petra J., additional, Ramos Mozo, Priscila, additional, González-Armengol, Juan J., additional, González del Castillo, Juan M., additional, Martín Sánchez, Javier, additional, Villarroel, Pedro, additional, Santiago, José L., additional, Bosch, Ricardo J., additional, Macaya, Carlos, additional, Esbrit, Pedro, additional, and López-Farré, Antonio J., additional

Published
2007
Full Text
View/download PDF

18. Relationship between Vitamin D Binding Protein and Aspirin Resistance in Coronary Ischemic Patients: A Proteomic Study

Author

López-Farré, Antonio J., primary, Mateos-Cáceres, Petra J., additional, Sacristán, Daniel, additional, Azcona, Luis, additional, Bernardo, Esther, additional, Perez de Prada, Teresa, additional, Alonso-Orgaz, Sergio, additional, Fernández-Arquero, Miguel, additional, Fernández-Ortiz, Antonio, additional, and Macaya, Carlos, additional

Published
2007
Full Text
View/download PDF

19. Direct Effect of F12511, A Systemic Inhibitor of Acyl-CoA Cholesterol Acyltransferase on Bovine Aortic Endothelial Cells

Author

Zamorano-León, José J, primary, Fernández-Sánchez, Ruth, additional, López Farré, Antonio J, additional, Lapuente-Tiana, Lucía, additional, Alonso-Orgaz, Sergio, additional, Sacristán, Daniel, additional, Junquera, Didier, additional, Delhon, André, additional, Conesa, Antonio, additional, Mateos-Cáceres, Petra J, additional, and Macaya, Carlos, additional

Published
2006
Full Text
View/download PDF

20. Proteomic Study of Plasma from Moderate Hypercholesterolemic Patients

Author

Alonso-Orgaz, Sergio, primary, Moreno, Laura, additional, Macaya, Carlos, additional, Rico, Luis, additional, Mateos-Cáceres, Petra J., additional, Sacristán, Daniel, additional, Pérez-Vizcaíno, Francisco, additional, Segura, Antonio, additional, Tamargo, Juan, additional, and López-Farré, Antonio, additional

Published
2006
Full Text
View/download PDF

22. Old and New Molecular Mechanisms Associated with Platelet Resistance to Antithrombotics.

Author

Farré, Antonio J. López, Tamargo, Juan, Mateos-Cáceres, Petra J., Azcona, Luís, and Macaya, Carlos

Subjects
MOLECULES, BLOOD platelets, ANTICOAGULANTS, PLATELET aggregation inhibitors, ASPIRIN
Abstract

Current available data show that about 5 to 40% of coronary patients treated with conventional doses of antithrombotic drugs do not display adequate antiplatelet response. Nowadays, aspirin remains the main antiplatelet therapy. However, a significant number of patients show platelet resistance to aspirin therapy, and recurrent thrombotic events occur. Combined antithrombotic therapies with thienopyridines, such as clopidogrel have been used to resolve this problem. However, clopidogrel treatment has been also associated with wide response variability, and non-responsiveness to clopidogrel also occurs in some patients. Therefore, the main question arising about the antithrombotic therapy is why particular patients do not benefit from the therapy and how they might be identified to improve their treatment. Different hypotheses have been suggested, including genetic factors, platelet heterogeneity, non-compliance and others. However, it is probably that many molecular mechanisms involved in platelet resistance to antithrombotic therapies still remains unknown. New technologies, such as proteomics and genetic, are beginning to show new unknown biological biomarkers and molecular mechanisms which may be associated with platelet antithrombotic drug resistance. [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

23. A Proteomic Approach to Determine Changes in Proteins Involved in the Myocardial Metabolism in Left Ventricles of Spontaneously Hypertensive Rats.

Author

Zamorano-León, Jose J., Modrego, Javier, Mateos-Cáceres, Petra J., Macaya, Carlos, Martín-Fernández, Beatriz, Miana, María, De las Heras, Natalia, Cachofeiro, Victoria, Lahera, Vicente, and López-Farré, Antonio J.

Subjects
PROTEOMICS, PROTEINS, HEART metabolism, LEFT heart ventricle, HYPERTENSION, GLYCOLYSIS, LABORATORY rats
Abstract

Background: Different works have suggested that in the hypertrophied heart the energy metabolic pathway shifts to glycolysis. Our aim was to evaluate using proteomics the expression of proteins associated with different energetic metabolic pathways in hypertrophied left ventricles of spontaneously hypertensive rats (SHR). Methods: 24-weeks-old SHR with stable hypertension and established left ventricle hypertrophy were used. Normotensive Wistar Kyoto rats were used as control. Proteins from left ventricles were analyzed by 2-dimensional electrophoresis and identified by comparison with a virtual rat heart proteomic map and mass spectrometry. Results: Enoyl-CoA hydratase expression, an enzyme involved in fatty acid β-oxidation, was reduced whereas the expression of other β-oxidation enzymes, 3-ketoacyl-CoA thiolase and the mitochondrial precursor of acyl-CoA thioester hydrolase, was increased in the hypertrophied left ventricles. The expression of two enzymes involved in the first steps of glycolysis, fructose bisphosphate aldolase and triosephosphate isomerase, was reduced in the left ventricle of SHR. Pyruvate dehydrogenase expression, enzyme involved in glucose oxidation, was enhanced in the hypertrophied ventricles whereas proteins of the tricarboxylic acid cycle were not modified. Proteins involved in the mitochondrial oxidative phosphorylation were overexpressed whereas the α-subunit of the mitochondrial precursor of ATP synthase was downexpressed. Conclusions: Several proteins involved in the main energy metabolic pathways were up and downexpressed. Moreover, our results seem to suggest that probably neither fatty acid β-oxidation nor glycolysis are the only sources for energy in the hypertrophied left ventricle. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

25. Effect of C-reactive protein on Fcγ receptor II in cultured bovine endothelial cells

Author

ESCRIBANO-BURGOS, Marta, LÓPEZ-FARRÉ, Antonio, del MAR GONZÁLEZ, María, MACAYA, Carlos, GARCÍA-MÉNDEZ, Antonio, MATEOS-CÁCERES, Petra J., ALONSO-ORGAZ, Sergio, CARRASCO, Carolina, RICO, Luis A., and PORRES CUBERO, Juan Carlos

Abstract

The major CRP (C-reactive protein) receptor on leucocytes has been identified as the low-affinity IgG receptor Fcγ receptor II (CD32). Our aim was to assess whether inflammation may modify the presence of the CD32 receptor in BAEC (bovine aortic endothelial cells). Confocal microscopy experiments showed a weak expression of the CD32 receptor in control BAEC that was slightly increased by 10 μg/ml CRP. Incubation of BAEC with TNF-α (tumour necrosis factor-α) did not modify the fluorescence signal of CD32. Addition of CRP to TNF-α-incubated BAEC enhanced the fluorescence signal of the CD32 receptors. The CD32 receptors showed a perinuclear cytoplasmic localization in BAEC. An alteration of the NO (nitric oxide)-dependent vasorelaxation has been defined as endothelial dysfunction. Endothelial dysfunction has been associated with the presence of superoxide anion and with a reduction in the expression of the eNOS (endothelial NO synthase). A concentration of CRP similar to that detected in patients with cardiovascular risk (10 μg/ml) failed to modify the generation of superoxide anion stimulated by TNF-α. Western blot experiments showed that TNF-α decreased the expression of the eNOS protein, which was partially protected by treatment with 10 μg/ml CRP. The protective effect of 10 μg/ml CRP on eNOS expression in TNF-α-incubated BAEC was prevented by an antibody against CD32 receptors. In conclusion, the present results suggest that, although CRP has been associated with inflammation, CRP may protect the expression of eNOS protein against pro-inflammatory mediators such as TNF-α.

Published
2005
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results