Browsing by Author "Lavandero, Sergio"
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- ItemÁcido úrico: una molécula con acciones paradójicas en la insuficiencia cardiaca(2011) Alcaíno, Hernán; Greig, Douglas; Castro Gálvez, Pablo Federico; Verdejo Pinochet, Hugo; Mellado Suazo, Rosemarie; García, Lorena; Díaz Araya, Guillermo; Quiroga Lagos, Clara Rosa; Chiong, Mario; Lavandero, Sergio
- ItemAcute effect of iloprost inhalation on right atrial function and ventricular dyssynchrony in patients with pulmonary artery hypertension(2017) Gabrielli, Luigi; Ocaranza, María Paz; Sitges, Marta; Kanacri, Andrés; Saavedra Madariaga, Rodrigo Alejandro; Sepúlveda, Pablo; Sepúlveda, Luis; Rossel, Víctor; Zagolin, Mónica; Verdejo Pinochet, Hugo; Baraona Reyes, Fernando Exequiel; Zalaquett Sepúlveda, Ricardo; Chiong, Mario; Lavandero, Sergio; Castro Gálvez, Pablo Federico
- ItemAngiotensin II-Regulated Autophagy Is Required for Vascular Smooth Muscle Cell Hypertrophy(2019) Mondaca-Ruff, David; Riquelme, Jaime A.; Quiroga Lagos, Clara Rosa; Norambuena-Soto, Ignacio; Sanhueza-Olivares, Fernanda; Villar-Fincheira, Paulina; Hernández-Díaz,Tomás; Cancino-Arenas, Nicole; San Martín, Alejandra; García, Lorena; Lavandero, Sergio; Chiong, Mario
- ItemAngiotensin-(1-9) reduces cardiovascular and renal inflammation in experimental renin-independent hypertension(2018) Gonzalez, Leticia; Novoa, Ulises; Moya, Jackeline; Gabrielli, Luigi; Jalil Milad, Jorge; Garcia, Lorena; Chiong, Mario; Lavandero, Sergio; Paz Ocaranza, Maria
- ItemAngiotensin-(1-9) regulates cardiac hypertrophy in vivo and in vitro(LIPPINCOTT WILLIAMS & WILKINS, 2010) Paz Ocaranza, Maria; Lavandero, Sergio; Jalil, Jorge E.; Moya, Jaqueline; Pinto, Melissa; Novoa, Ulises; Apablaza, Felipe; Gonzalez, Leticia; Hernandez, Carol; Varas, Manuel; Lopez, Rene; Godoy, Ivan; Verdejo, Hugo; Chiong, MarioBackground Angiotensin-(1-9) is present in human and rat plasma and its circulating levels increased early after myocardial infarction or in animals treated with angiotensin-converting enzyme inhibitor. However, the cardiovascular effects of this peptide are unknown.
- Itembeta-Hydroxybutyrate Increases Exercise Capacity Associated with Changes in Mitochondrial Function in Skeletal Muscle(MDPI, 2020) Monsalves Alvarez, Matias; Morales, Pablo Esteban; Castro Sepulveda, Mauricio; Sepulveda, Carlos; Rodriguez, Juan Manuel; Chiong, Mario; Eisner, Veronica; Lavandero, Sergio; Troncoso, Rodrigobeta-hydroxybutyrate is the main ketone body generated by the liver under starvation. Under these conditions, it can sustain ATP levels by its oxidation in mitochondria. As mitochondria can modify its shape and function under different nutritional challenges, we study the chronic effects of beta-hydroxybutyrate supplementation on mitochondrial morphology and function, and its relation to exercise capacity. Male C57BL/6 mice were supplemented with beta-hydroxybutyrate mineral salt (3.2%) or control (CT, NaCl/KCl) for six weeks and submitted to a weekly exercise performance test. We found an increase in distance, maximal speed, and time to exhaustion at two weeks of supplementation. Fatty acid metabolism and OXPHOS subunit proteins declined at two weeks in soleus but not in tibialis anterior muscles. Oxygen consumption rate on permeabilized fibers indicated a decrease in the presence of pyruvate in the short-term treatment. Both the tibialis anterior and soleus showed decreased levels of Mitofusin 2, while electron microscopy assessment revealed a significant reduction in mitochondrial cristae shape in the tibialis anterior, while a reduction in the mitochondrial number was observed only in soleus. These results suggest that short, but not long-term, beta-hydroxybutyrate supplementation increases exercise capacity, associated with modifications in mitochondrial morphology and function in mouse skeletal muscle.
- ItemCirculating Vascular Cell Adhesion Molecule-1 (sVCAM-1) Is Associated With Left Atrial Remodeling in Long-Distance Runners(FRONTIERS MEDIA SA, 2021) Contreras Briceño, Felipe; Herrera, Sebastián; Vega Adauy, Julián; Salinas, Manuel; Ocaranza Jeraldino, María Paz; Jalil Milad, Jorge; Mandiola Ovalle, Jorge; García, Lorena; Chiong, Mario; Castro Galvez, Pablo Federico; Lavandero, Sergio; Gabrielli Nervi, Luigi ArnaldoIntroduction: An increased risk of atrial fibrillation (AF) has been demonstrated in high-performance athletes. Soluble vascular adhesion molecule-1 (sVCAM-1), a biomarker involved in inflammation and cardiac remodeling, is associated with the development of AF in the general population. However, the relationship between sVCAM-1 and left atrial (LA) remodeling has been poorly investigated in long-distance runners (LDR).Aim: To determine the association between LA remodeling and sVCAM-1 levels in LDR during the training period before a marathon race.Methods: Thirty-six healthy male LDR (37.0 +/- 5.3 years; 174.0 +/- 7.0 height; BMI: 23.8 +/- 2.8; V degrees O-2-peak: 56.5 +/- 7.3 mL center dot kg(-1)center dot min(-1)) were evaluated in this single-blind and cross-sectional study. The LDR were separated into two groups according to previous training levels: high-training (HT) (n = 18) >= 100 km center dot week(-1) and low-training (LT) (n = 18) >= 70 and <100 km center dot week(-1). Also, 18 healthy non-active subjects were included as a control group (CTR). In all participants, transthoracic echocardiography was performed. sVCAM-1 blood levels were measured baseline and immediately finished the marathon race in LDR.Results: HT showed increased basal levels of sVCAM-1 (651 +/- 350 vs. 440 +/- 98 ng center dot mL(-1) CTR, p = 0.002; and vs. 533 +/- 133 ng center dot mL(-1) LT; p = 0.003) and a post-marathon increase (Delta sVCAM-1) (651 +/- 350 to 905 +/- 373 ng center dot mL(-1); p = 0.002), that did not occur in LT (533 +/- 133 to 651 +/- 138 ng center dot mL(-1); p = 0.117). In LDR was a moderate correlation between LA volume and sVCAM-1 level (rho = 0.510; p = 0.001).Conclusions: In male long-distance runners, sVCAM-1 levels are directly associated with LA remodeling. Also, the training level is associated with basal sVCAM-1 levels and changes after an intense and prolonged exercise (42.2 km). Whether sVCAM-1 levels predict the risk of AF in runners remains to be established.
- ItemCounter-regulatory renin–angiotensin system in cardiovascular disease(2019) Ocaranza, María Paz; Riquelme, Jaime A.; García, Lorena; Jalil Milad, Jorge; Chiong, Mario; Santos, Robson A. S.; Lavandero, Sergio
- ItemDexmedetomidine preconditioning activates pro-survival kinases and attenuates regional ischemia/reperfusion injury in rat heart(ELSEVIER, 2012) Ibacache, Mauricio; Sanchez, Gina; Pedrozo, Zully; Galvez, Felipe; Humeres, Claudio; Echevarria, Ghislaine; Duaso, Juan; Hassi, Mario; Garcia, Lorena; Diaz Araya, Guillermo; Lavandero, SergioPharmacological preconditioning limits myocardial infarct size after ischemia/reperfusion. Dexmedetomidine is an alpha(2)-adrenergic receptor agonist used in anesthesia that may have cardioprotective properties against ischemia/reperfusion injury. We investigate whether dexmedetomidine administration activates cardiac survival kinases and induces cardioprotection against regional ischemia/reperfusion injury. In in vivo and ex vivo models, rat hearts were subjected to 30 min of regional ischemia followed by 120 min of reperfusion with dexmedetomidine before ischemia. The alpha(2)-adrenergic receptor antagonist yohimbine was also given before ischemia, alone or with dexmedetomidine. Erk1/2, Akt and eNOS phosphorylations were determined before ischemia/reperfusion. Cardioprotection after regional ischemia/reperfusion was assessed from infarct size measurement and ventricular function recovery. Localization of alpha(2)-adrenergic receptors in cardiac tissue was also assessed. Dexmedetomidine preconditioning increased levels of phosphorylated Erk1/2, Akt and eNOS forms before ischemia/reperfusion; being significantly reversed by yohimbine in both models. Dexmedetomidine preconditioning (in vivo model) and pen-insult protection (ex vivo model) significantly reduced myocardial infarction size, improved functional recovery and yohimbine abolished dexmedetomidine-induced cardioprotection in both models. The phosphatidylinositol 3-kinase inhibitor LY-294002 reversed myocardial infarction size reduction induced by dexmedetomidine preconditioning. The three isotypes of alpha(2)-adrenergic receptors were detected in the whole cardiac tissue whereas only the subtypes 2A and 2C were observed in isolated rat adult cardiomyocytes. These results show that dexmedetomidine preconditioning and dexmedetomidine pen-insult administration produce cardioprotection against regional ischemia/reperfusion injury, which is mediated by the activation of pro-survival kinases after cardiac alpha(2)-adrenergic receptor stimulation. (C) 2011 Elsevier B.V. All rights reserved.
- ItemDissociating angiotensin 1-9 anticardiovascular remodeling effects from those on blood pressure(2014) Ocaranza, María Paz; Michea, Luis; Chiong, Mariod; Lavandero, Sergio; Jalil Milad, Jorge
- ItemDown syndrome critical region 1 gene, rcan1, helps maintain a more fused mitochondrial network(2018) Parra, Valentina; Altamirano, Francisco; Hernández Fuentes, Carolina P.; Tong, Dan; Kyrychenko, Victoriia; Rotter, David; Pedrozo, Zully; Hill, Joséph A.| Eisner Sagüés, Verónica Raquel; Lavandero, Sergio; Schneider, Jay W.; Rothermel, Beverly A.
- ItemEffects of atorvastatin therapy in heart failure: Oxidative stress, inflammation, endothelial dysfunction and exercise capacity(ELSEVIER SCIENCE INC, 2007) Miranda, Rodrigo; Castro, Pablo; Verdejo, Hugo; Greig, Douglas; Alcaino, Hernan; Bustos, Carlos; Vukasovic, Jose Luis; Godoy, Ivan; Diaz Araya, Guillermo; Lavandero, Sergio
- ItemEnalapril attenuates downregulation of angiotensin-converting enzyme 2 in the late phase of ventricular dysfunction in myocardial infarcted rat(LIPPINCOTT WILLIAMS & WILKINS, 2006) Ocaranza, Maria Paz; Godoy, Ivan; Jalil, Jorge E.; Varas, Manuel; Collantes, Patricia; Pinto, Melissa; Roman, Maritza; Ramirez, Cristian; Copaja, Miguel; Diaz Araya, Guillermo; Castro, Pablo; Lavandero, SergioThe early and long-term effects of coronary artery ligation on the plasma and left ventricular angiotensin-converting enzyme (ACE and ACE2) activities, ACE and ACE2 mRNA levels, circulating angiotensin (Ang) levels [Ang I, Ang-(1-7), Ang-(1-9), and Ang II], and cardiac function were evaluated 1 and 8 weeks after experimental myocardial infarction in adult Sprague Dawley rats. Sham-operated rats were used as controls. Coronary artery ligation caused myocardial infarction, hypertrophy, and dysfunction 8 weeks after surgery. At week 1, circulating Ang II and Ang-(1-9) levels as well as left ventricular and plasma ACE and ACE2 activities increased in myocardial-infarcted rats as compared with controls. At 8 weeks post-myocardial infarction, circulating ACE activity, ACE mRNA levels, and Ang II levels remained higher, but plasma and left ventricular ACE2 activities and mRNA levels and circulating levels of Ang-(1-9) were lower than in controls. No changes in plasma Ang-(1-7) levels were observed at any time. Enalapril prevented cardiac hypertrophy and dysfunction as well as the changes in left ventricular ACE, left ventricular and plasmatic ACE2, and circulating levels of Ang II and Ang-(1-9) after 8 weeks postinfafction. Thus, the decrease in ACE2 expression and activity and circulating Ang-(1-9) levels in late ventricular dysfunction post-myocardial infarction were prevented with enalapril. These findings suggest that in this second arm of the renin-angiotensin system, ACE2 may act through Ang-(1-9), rather than Ang-(1-7), as a counterregulator of the first arm, where ACE catalyzes the formation of Ang II.
- ItemEnergy-preserving effects of IGF-1 antagonize starvation-induced cardiac autophagy(2012) Troncoso, Rodrigo; Vicencio, Jose Miguel; Parra, Valentina; Nemchenko, Andriy; Kawashima, Yuki; Del Campo, Andrea; Toro, Barbra; Battiprolu, Pavan K.; Aranguiz, Pablo; Chiong, Mario; Yakar, Shoshana; Gillette, Thomas G.; Hill, Joseph A.; Abel, Evan Dale; LeRoith, Derek; Lavandero, Sergio
- ItemER-to-mitochondria miscommunication and metabolic diseases(2015) López Crisosto, Camila; Bravo Sagua, Roberto; Rodriguez Peña, Marcelo; Mera, Claudia; Castro Gálvez, Pablo Federico; Quest, Andrew F. G.; Rothermel, Beverly A.; Cifuentes, Mariana; Lavandero, Sergio
- ItemImpaired cardiac autophagy in patients developing postoperative atrial fibrillation(MOSBY-ELSEVIER, 2012) Garcia, Lorena; Verdejo, Hugo E.; Kuzmicic, Jovan; Zalaquett, Ricardo; Gonzalez, Sergio; Lavandero, Sergio; Corbalan, RamonObjectives: Postoperative atrial fibrillation (POAF) is a common complication after on-pump heart surgery. Several histologic abnormalities, such as interstitial fibrosis and vacuolization, have been described in atrial samples from patients developing POAF. This ultrastructural remodeling has been associated with the establishment of a proarrhythmic substrate. We studied whether atrial autophagy is activated in patients who develop POAF.
- ItemIncreased active phase atrial contraction is related to marathon runner performance(2018) Gabrielli, Luigi; Herrera, Sebastián; Contreras Briceño, Felipe; Vega, Julián; Ocaranza, María Paz; Yáñez Díaz, Fernando; Fernández, Rodrigo; Saavedra Madariaga, Rodrigo Alejandro; Sitges, Marta; García, Lorena; Chiong, Mario; Lavandero, Sergio; Castro Gálvez, Pablo Federico
- ItemIncreased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress(COMPANY BIOLOGISTS LTD, 2011) Bravo, Roberto; Miguel Vicencio, Jose; Parra, Valentina; Troncoso, Rodrigo; Pablo Munoz, Juan; Bui, Michael; Quiroga, Clara; Rodriguez, Andrea E.; Verdejo, Hugo E.; Ferreira, Jorge; Iglewski, Myriam; Chiong, Mario; Simmen, Thomas; Zorzano, Antonio; Hill, Joseph A.; Rothermel, Beverly A.; Szabadkai, Gyorgy; Lavandero, SergioIncreasing evidence indicates that endoplasmic reticulum (ER) stress activates the adaptive unfolded protein response (UPR), but that beyond a certain degree of ER damage, this response triggers apoptotic pathways. The general mechanisms of the UPR and its apoptotic pathways are well characterized. However, the metabolic events that occur during the adaptive phase of ER stress, before the cell death response, remain unknown. Here, we show that, during the onset of ER stress, the reticular and mitochondrial networks are redistributed towards the perinuclear area and their points of connection are increased in a microtubule-dependent fashion. A localized increase in mitochondrial transmembrane potential is observed only in redistributed mitochondria, whereas mitochondria that remain in other subcellular zones display no significant changes. Spatial re-organization of these organelles correlates with an increase in ATP levels, oxygen consumption, reductive power and increased mitochondrial Ca2+ uptake. Accordingly, uncoupling of the organelles or blocking Ca2+ transfer impaired the metabolic response, rendering cells more vulnerable to ER stress. Overall, these data indicate that ER stress induces an early increase in mitochondrial metabolism that depends crucially upon organelle coupling and Ca2+ transfer, which, by enhancing cellular bioenergetics, establishes the metabolic basis for the adaptation to this response.
- ItemIncreased levels of oxidative stress, subclinical inflammation, and myocardial fibrosis markers in primary aldosteronism patients(2010) Stehr, Carlos B.; Mellado Suazo, Rosemarie; Ocaranza, María Paz; Carvajal Maldonado, Cristián Andrés; Mosso Gómez, Lorena; Becerra, Elia; Solis, Margarita; Garcia, Lorena; Lavandero, Sergio; Jalil Milad, Jorge; Fardella B., Carlos
- ItemIncreased Oxidative Stress Correlates With Pulmonary Vascular Response to Vasodilators in Pulmonary Artery Hypertension Patients(2009) Castro Gálvez, Pablo Federico; Gabrielli, Luigi; Fasce, Fabrizio; |Verdejo Pinochet, Hugo; Greig, Douglas; Llevaneras, Silvana; Ferrada, Marcela; Hernandez, Claudia; Godoy J., Iván; Garcia, Lorena; Mellado Suazo, Rosemarie; Sepulveda, Pablo; Lavandero, Sergio
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