Person:
Álvarez Llamas, Gloria

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First Name
Gloria
Last Name
Álvarez Llamas
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Ciencias Químicas
Department
Bioquímica y Biología Molecular
Area
Bioquímica y Biología Molecular
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Now showing 1 - 3 of 3
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    Modification of the Secretion Pattern of Proteases, Inflammatory Mediators, and Extracellular Matrix Proteins by Human Aortic Valve is Key in Severe Aortic Stenosis
    (Molecular and cellular proteomics, 2013) Álvarez Llamas, Gloria; Martín Rojas, Tatiana; Cuesta, Fernando De La; Calvo, Enrique; Gil Dones, Félix; Dardé, Veronica ; López Almodovar, Luis ; Padial, Luis ; Lopez, Juan Antonio; Vivanco Martínez, Fernando; Barderas, Maria
    One of the major challenges in cardiovascular medicine is to identify candidate biomarker proteins. Secretome analysis is particularly relevant in this search as it focuses on a subset of proteins released by a cell or tissue under certain conditions. The sample can be considered as a plasma subproteome and it provides a more direct approximation to the in vivo situation. Degenerative aortic stenosis is the most common worldwide cause of valve replacement. Using a proteomic analysis of the secretome from aortic stenosis valves we could identify candidate markers related to this pathology, which may facilitate early diagnosis and treatment. For this purpose, we have designed a method to validate the origin of secreted proteins, demonstrating their synthesis and release by the tissue and ruling out blood origin. The nLC-MS/MS analysis showed the labeling of 61 proteins, 82% of which incorporated the label in only one group. Western blot and selective reaction monitoring differential analysis, revealed a notable role of the extracellular matrix. Variation in particular proteins such as PEDF, cystatin and clusterin emphasizes the link between aortic stenosis and atherosclerosis. In particular, certain proteins variation in secretome levels correlates well, not only with label incorporation trend (only labeled in aortic stenosis group) but, more importantly, with alterations found in plasma from an independent cohort of samples, pointing to specific candidate markers to follow up in diagnosis, prognosis, and therapeutic intervention.
  • Item
    Proteomics - A Powerful Tool to Deepen the Molecular Mechanisms of Aortic Stenosis Disease
    (Aortic Stenosis - Etiology, Pathophysiology and Treatment, 2011) Gil Dones, Félix; Cuesta, Fernando de la; Álvarez Llamas, Gloria; Padial, Luis ; López-Almodovar, Luis ; Martin-Rojas, Tatiana; Vivanco, Fernando; Barderas, Maria
  • Item
    Analysis of the Plasma Proteome Associated with Acute Coronary Syndrome: Does a Permanent Protein Signature Exist in the Plasma of ACS Patients?
    (Journal of protemoe research, 2010) Dardé, Veronica ; Cuesta, Fernando de la; Gil Dones, Félix; Álvarez Llamas, Gloria; Barderas, Maria ; Vivanco Martínez, Fernando
    Acute coronary syndrome (ACS) is triggered by the occlusion of a coronary artery usually due to the thrombosis caused by an atherosclerotic plaque. The identification of proteins directly involved in the pathophysiological events underlying ACS will enable more precise diagnoses and a more accurate prognosis to be determined. Accordingly, we have performed a longitudinal study of the plasma proteome in ACS patients by 2-DE and DIGE. Plasma samples from patients, healthy controls, and stable coronary artery disease (CAD) patients were immunodepleted of the six most abundant proteins, and they were analyzed in parallel at four different times: 0 (on admission) and after 4, 60, and 180 days. From a total of 1400 spot proteins analyzed, 33 proteins were differentially expressed in ACS patients when compared with control subjects/stable patients. A small group of seven proteins that appear to be altered at admission remain affected for 6 months and also in the stable CAD patients. Interestingly, the maximum number of altered proteins was observed in the stable CAD patients. Some of the proteins identified had been previously associated with ACS whereas others (such as Alpha-1-B-glycoprotein, Hakata antigen, Tetranectin, Tropomyosin 4) constitute novel proteins that are altered in this pathology.