Browsing by Author "Panes Becerra, Olga Teresa"

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    An adenine insertion in exon 6 of human GP6 generates a truncated protein associated with a bleeding disorder in four Chilean families
    (2013) Matus Ritter, Valeria; Valenzuela, G.; Sáez S., Claudia; Hidalgo, P.; Lagos Lucero, Marcela; Aranda Lauriani, Eduardo Javier; Panes Becerra, Olga Teresa; Pereira Garcés, Jaime Ignacio; Pillois, X.; Nurden, A.; Mezzano, Diego
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    Atorvastatin Prevents the Proadhesive and Prothrombotic Endothelial Cell Phenotype Induced by Cocaine and Plasma from Cocaine Consumers in Vitro
    (2014) Sáez, C.; Pereira Flores, K.; Ebensperger González, Roberto Alejandro; Panes Becerra, Olga Teresa; Massardo, T.; Hidalgo, P.; Mezzano, Diego; Pereira Garcés, Jaime Ignacio
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    La atorvastatina no modifica el incremento agudo de los niveles de p-selectina y fibrinógeno inducido con esfuerzo físico máximo
    (2010) Lindefjeld, Dante; Acevedo B., Mónica; Chamorro S., Gastón; Mezzano, Diego; Panes Becerra, Olga Teresa; Aranis, C.; Oporto, J.
    Introducción: Las estatinas han demostrado disminuir los eventos cardiovasculares en sujetos con y sin enfermedad aterosclerótica establecida. Se ha demostrado, que sus efectos benéficos no sólo dependen de la reducción del colesterol, sino que también podrían ser secundarios a otros efectos de las estatinas, como su efectos de reducción de inflamación y/ o trombogénesis entre otros. Sin embargo, no existen trabajos que demuestren que las estatinas sean capaces de frenarla activación de la cascada de inflamación y/o trombogénesis. Objetivos: Determinar el efecto de la administración oral de atorvastatina por 7 días sobre los niveles plasmáticos de proteína C- reactiva ultrasensible (PCR us), fibrinógeno y P-selectina, pre y post prueba de esfuerzo máximo inmediato y a las 24 horas de su ejecución. Métodos: Ensayo clínico en 50 hombres sanos (18 a 50 años), randomizado atorvastatina 80 mg/día - placebo por 7 días, doble ciego. Muestras tomadas en sangre para PCRus, fibrinógeno y P-selectina, perfil lipídico, creatin kinasa y transaminasas hepáticas, pre y post test de esfuerzo, y a las 24 horas. Los resultados para datos continuos se expresan como medias ± desviación estándar, test de student para muestras independientes, ANOVA para muestras repetidas. Programa estadístico SPSS 14.0. Resultados: Un grupo de 44 sujetos completaron el estudio: atorvastatina 80 mg (n=24) o placebo (n=20). En el grupo atorvastatina, después de una semana de tratamiento, los niveles de LDLc disminuyeron en 38% (LDL basal: 97 ± 27 mg/dL vs LDL post: 62 ± 31 mg/dL, p < 0.001). Sin embargo, no se observaron cambios en ese mismo período en los niveles de PCRus, fibrinógeno y P-selectina con respecto a placebo. Los niveles de fibrinógeno se elevaron 8% entre la etapa pre y post ejercicio inmediato (341 ± 56 mg/dL vs 368 ± 65 mg/dL, p<0.001), retornando a los niveles básales a las 24 horas; no hubo diferencias entre atorvastatina - placebo. Los niveles de P-selectina aumentaron 9.5% entre la etapa pre y post ejercicio inmediato (25 ± 1.5 ng/dL vs 28 ±1.7 ng/dL, p = 0.01), retornando a los niveles basales a las 24 horas; no hubo diferencias entre atorvastatina - placebo. El ejercicio no indujo elevación de PCRus. Los niveles plasmáticos de CKtotal se elevaron significativamente en ambos grupos post ejercicio (Atorvastatina 43% aumento, p = 0.004 versus nivel basal y placebo 12% aumento, p = 0.005 versus nivel basal). Sin embargo, no se encontró diferencias estadísticamente significativas entre el grupo atorvastatina versus placebo. Conclusiones: La administración de atorvastatina oral 80 mg/día por 7 días en sujetos sanos no inhibió la elevación de los niveles plasmáticos de fibrinógeno y P-selectina inducida por ejercicio.
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    Complementary effects of Mediterranean diet and moderate red wine intake on haemostatic cardiovascular risk factors
    (NATURE PUBLISHING GROUP, 2001) Mezzano, Diego; Leighton Puga, Federico; Martínez, Carlos; Marshall Rivera, Guillermo; Cuevas Marín, Ada Marisa; Castillo Valenzuela, Oscar; Panes Becerra, Olga Teresa; Rozowski Narkunska, Samuel Jaime; Pérez Pons, Druso Diego; Mizón Costa, Claudio Luis Enrique; San Martin, Alejandra; Pereira Pereira, J. Marcello
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    Daño endotelial y activación del sistema hemostático asociado al uso crónico de cocaína: estudios ex vivo e in vitro
    (2010) Pereira Garcés, Jaime Ignacio; Sáez, C.; Olivares, P.; Moreno, N.; Cabrera, M. J.; Panes Becerra, Olga Teresa; Belmont, S.; Hidalgo, P.; Massardo, T.; Pallavicini, J.; Mezzano, Diego
    Antecedentes: Usuarios crónicos de cocaína tienen riesgo aumentado de presentar infarto de miocardio, angina, muerte súbita y accidentes cerebrovasculares. Aunque la patogenia del daño vascular es mayormente desconocida, se ha encontrado arterieesclerosis prematura y formación de trombos intravasculares. Objetivo: Demostrar evidencia de daño endotelial y activación del sistema hemostático en usuarios crónicos de cocaína. Métodos: Un grupo de 23 pacientes con criterios de dependencia a cocaína DSM-IV; 19 hombres (edad promedio 32 a), con exposición a la droga dentro de 72 h del estudio. Disfunción endotelial se evaluó por enumeración de las células endoteliales circulantes (CEC) y nivel de sICAM . Para activación del sistema hemostático se incluyó: complejos trombina-antitrombina (TAT) y generación de trombina; NAP-2 y RANTES para activación plaquetaria. In vitro, CE en cultivo (HUVEC), se expusieron a plasma de consumidores o controles. Se midió factor von Willebrand (FVW) en el medio y expresión de FvW y factor tisú lar (FT) sobre las CE. adhesion plaquetaria estática se evaluó por microscopía. Resultados: En usuarios de cocaína, con respecto a controles, las CEC estaban significativamente elevadas (63±28 vs 7±5 células/mL; p<0. 0001), así como los niveles plasmáticos de sICAM (360±92 vs 261 ±34 ng/mL, respectivamente; p<0. 01). TAT en pacientes y controles fueron 2. 7±0. 7 y 0. 7±0. 4µg/L; p<0. 06). NAP-2 (129±8. 4 ng/mL) y RANTES (4. 01 ±2. 12 ng/mL) significativamente aumentados comparados con controles (87. 1 ±8. 6 añd 2. 12±0. 35, respectivamente; p< 0. 01). El plasma de usuarios de cocaína indujo mayor liberación de FVW desde las HUVEC comparado con plasma control (5. 64±4. 0 vs 1. 4±0. 8 UI/dL; p ≤ 0. 001). Las HUVEC expuestas a estos mismos plasmas, mostraron aumento significativo en la expresión de FT, FVW y mayor capacidad de adherir plaquetas. Conclusiones: Consumidores crónicos de cocaína evidencian disfunción endotelial y activación del sistema hemostático. En conjunto con las observaciones in vitro del efecto de los plasmas sobre las CE, estos resultados sugieren que la aterotrombosis puede jugar un papel importante en la patogenia del daño vascular asociado al uso de cocaína.
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    Diagnosis of mild platelet function disorders. Reliability and usefulness of light transmission platelet aggregation and serotonin secretion assays
    (2009) Quiroga Gutiérrez, Sara Teresita; Goycolea, Manuela; Matus Ritter, Valeria; Zúñiga Contreras, Pamela; Martínez, Carlos; Garrido, Marcelo; Aranda Lauriani, Eduardo Javier; Leighton Puga, Federico; Panes Becerra, Olga Teresa; Pereira Garcés, Jaime Ignacio; Mezzano, Diego
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    Evaluation of oral anticoagulation with rivaroxaban, in patients with new onset non valvular atrial fibrillation
    (2016) Neira, V.; Corbalán Herreros, Ramón; Pereira Garcés, Jaime Ignacio; Panes Becerra, Olga Teresa; Garayar Pulgar, Bernardita; Aizman, Andrés; Llevaneras, S.; Villarroel del Pino, Luis A.
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    Genotype-phenotype relationship for six common polymorphisms in genes affecting platelet function from 286 healthy subjects and 160 patients with mucocutaneous bleeding of unknown cause
    (2009) Martínez, Constantino; Antón, Ana Isabel; Corral, Javier; Quiroga Gutiérrez, Sara Teresita; Panes Becerra, Olga Teresa; Lozano, María Luisa; González Conejero, Rocío; Teruel, Raúl; Navarro Núñez, Leyre; Pereira Garcés, Jaime Ignacio; Mezzano, Diego; Vicente, Vicente; Rivera, José
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    Human platelet interaction with E-coli O111 promotes tissue-factor-dependent procoagulant activity, involving Toll like receptor 4
    (2017) Matus, V.; Valenzuela, J.; Hidalgo, P.; Pozo, L.; Panes Becerra, Olga Teresa; Wozniak Banchero, Aniela; Mezzano, Diego; Pereira Garcés, Jaime Ignacio; Sáez, Claudia G.
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    Increased activation of protein C, but lower plasma levels of free, activated protein C in uraemic patients : relationship with systemic inflammation and haemostatic activation
    (BLACKWELL SCIENCE LTD, 2001) Mezzano, Diego; Quiroga Gutiérrez, Sara Teresita; Panes Becerra, Olga Teresa; Pereira Garcés, Jaime Ignacio; Pais, Edgar; Marshall Rivera, Guillermo; Tagle, Rodrigo; Downey Concha, Patricio; Cáceres, Soledad; González, Fernando
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    Inhibition of angiogenesis by platelets in systemic sclerosis patients
    (2015) Hirigoyen Pérez, Daniela María.; Burgos, Paula I.; Mezzano, Veronica.; Durán, Josefina; Barrientos, Magaly.; Sáez, Claudia G.; Panes Becerra, Olga Teresa; Mezzano, Diego; Iruretagoyena B., Mirentxu
    Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.Abstract Introduction Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by microvascular damage, inflammation, and fibrosis. It has become increasingly evident that platelets, beyond regulating hemostasis, are important in inflammation and innate immunity. Platelets may be an important source of proinflammatory and profibrotic cytokines in the vascular microenvironment. In this study, we sought to assess the contribution of platelet-derived factors in patients with SSc to the angiogenesis of human dermal microvascular endothelial cells (DMVECs) in a tubule formation assay and to characterize the secretion of profibrotic and proinflammatory cytokines in these platelets. Methods We analyzed platelets obtained from 30 patients with SSc and 12 healthy control subjects. Angiogenesis was evaluated in vitro with a DMVEC tubule formation assay on Matrigel and platelet-derived angiogenic factors such as vascular endothelial growth factor (VEGF), 165b isoform (VEGF165b), and cytokine secretion was evaluated. Platelet serotonin content was also determined. Results When DMVECs were incubated with SSc platelet releasates, tubule formation was significantly inhibited (p < 0.01, t test), and higher expression of endothelin-1 in these cells was observed compared with control subjects (p < 0.05, Mann–Whitney U test). In SSc platelet releasates, VEGF165b was significantly higher (p < 0.05, t test), and the VEGF165b/VEGF ratio was increased compared with that of control subjects. Higher secretion of transforming growth factor β (p < 0.01, t test) and CD40L (p < 0.01, t test) was observed compared with control subjects. Also, intraplatelet serotonin levels were lower in platelets obtained from patients with diffuse SSc compared with patients with limited SSc and control subjects (p < 0.05, t test). Conclusions Our findings suggest that antiangiogenic factors such as VEGF165b, together with proinflammatory and profibrotic factors secreted by platelets, can contribute to the progression of peripheral microvascular damage, defective vascular repair, and fibrosis in patients with SSc.
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    International collaborative study for the calibration of proposed International Standards for thromboplastin, rabbit, plain, and for thromboplastin, recombinant, human, plain
    (2017) Van den Besselaar, A.M.H P.; Chantarangkul, V.; Angeloni, F.; Binder, N. B.; Byrne, M.; Dauer, R.; Gudmundsdottir, B. R.; Jespersen, J.; Kitchen, S.; Panes Becerra, Olga Teresa
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    Platelet tissue factor activity and membrane cholesterol are increased in hypercholesterolemia and normalized by rosuvastatin, but not by atorvastatin.
    (2017) Panes Becerra, Olga Teresa; González, César; Hidalgo, Patricia; Valderas Igor, Juan Patricio; Acevedo B., Mónica; Contreras, Susana; Sánchez, Ximena; Pereira Garcés, Jaime Ignacio; Rigotti Rivera, Attilio; Mezzano, Diego
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    Platelets enhance tissue factor protein and metastasis initiating cell markers, and act as chemoattractants increasing the migration of ovarian cancer cells.
    (2015) Orellana, Renan.; Kato Cardemil, Sumie Rode; Erices, Rafaela.; Bravo Castillo, María Loreto; González Hevia, Pamela Andrea.; Oliva, Bárbara.; Cubillos Alfaro, Sofía María Jesús.; Valdivia Román, Andrés Felipe; Brañes, Jorge; Cuello F., Mauricio; Ibañez, Carolina; Barriga Cosmelli, María Isabel; Bravo, Erasmo.; Alonso, Catalina.; Bustamente, Eva.; Castellon, Enrique.; Hidalgo, Patricia.; Trigo, Cesar.; Panes Becerra, Olga Teresa; Pereira Garcés, Jaime Ignacio; Mezzano, Diego; Owen, Gareth Ivor
    Abstract Background An increase in circulating platelets, or thrombocytosis, is recognized as an independent risk factor of bad prognosis and metastasis in patients with ovarian cancer; however the complex role of platelets in tumor progression has not been fully elucidated. Platelet activation has been associated with an epithelial to mesenchymal transition (EMT), while Tissue Factor (TF) protein expression by cancer cells has been shown to correlate with hypercoagulable state and metastasis. The aim of this work was to determine the effect of platelet-cancer cell interaction on TF and “Metastasis Initiating Cell (MIC)” marker levels and migration in ovarian cancer cell lines and cancer cells isolated from the ascetic fluid of ovarian cancer patients. Methods With informed patient consent, ascitic fluid isolated ovarian cancer cells, cell lines and ovarian cancer spheres were co-cultivated with human platelets. TF, EMT and stem cell marker levels were determined by Western blotting, flow cytometry and RT-PCR. Cancer cell migration was determined by Boyden chambers and the scratch assay. Results The co-culture of patient-derived ovarian cancer cells with platelets causes: 1) a phenotypic change in cancer cells, 2) chemoattraction and cancer cell migration, 3) induced MIC markers (EMT/stemness), 3) increased sphere formation and 4) increased TF protein levels and activity. Conclusions We present the first evidence that platelets act as chemoattractants to cancer cells. Furthermore, platelets promote the formation of ovarian cancer spheres that express MIC markers and the metastatic protein TF. Our results suggest that platelet-cancer cell interaction plays a role in the formation of metastatic foci.
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    Quantitative impact of using different criteria for the laboratory diagnosis of type 1 von Willebrand disease
    (2014) Quiroga Gutiérrez, Sara Teresita; Goycoolea, M.; Belmont, S.; Panes Becerra, Olga Teresa; Aranda Lauriani, Eduardo Javier; Zúñiga, P.; Pereira Garcés, Jaime Ignacio; Mezzano, Diego