Browsing by Author "Garcia, Lorena"
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- 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
- ItemAutophagy and oxidative stress in non-communicable diseases: A matter of the inflammatory state?(2018) Pena-Oyarzun, Daniel; Bravo-Sagua, Roberto; Diaz-Vega, Alexis; Aleman, Larissa; Chiong, Mario; Garcia, Lorena; Bambs S., Claudia; Troncoso, Rodrigo; Cifuentes, Mariana; Morselli, Eugenia; Ferreccio Readi, Catterina; Quest, Andrew F. G.; Criollo, Alfred
- 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.
- ItemFibroblast Primary Cilia Are Required for Cardiac Fibrosis(2019) Villalobos, Elisa; Criollo, Alfredo; Schiattarella, Gabriele G.; Altamirano, Francisco; French, Kristin M.; May, Herman, I; Jiang, Nan; Ngoc Uyen Nhi Nguyen; Romero, Diego; Carlos Roa, Juan; Garcia, Lorena; Diaz-Araya, Guillermo; Morselli, Eugenia; Ferdous, Anwarul; Conway, Simon J.; Sadek, Hesham A.; Gillette, Thomas G.; Lavandero, Sergio; Hill, Joseph A.BACKGROUND: The primary cilium is a singular cellular structure that extends from the surface of many cell types and plays crucial roles in vertebrate development, including that of the heart. Whereas ciliated cells have been described in developing heart, a role for primary cilia in adult heart has not been reported. This, coupled with the fact that mutations in genes coding for multiple ciliary proteins underlie polycystic kidney disease, a disorder with numerous cardiovascular manifestations, prompted us to identify cells in adult heart harboring a primary cilium and to determine whether primary cilia play a role in disease-related remodeling.
- 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 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
- ItemMarkedly increased Rho-kinase activity in circulating leukocytes in patients with chronic heart failure(MOSBY-ELSEVIER, 2011) Paz Ocaranza, Maria; Gabrielli, Luigi; Mora, Italo; Garcia, Lorena; McNab, Paul; Godoy, Ivan; Braun, Sandra; Cordova, Samuel; Castro, Pablo; Novoa, Ulises; Chiong, Mario; Lavandero, Sergio; Jalil, Jorge E.Background The small guanosine triphosphatase Rho and its target Rho-kinase have significant roles in experimental remodeling and ventricular dysfunction, but no data are available on Rho-kinase activation in patients with heart failure (HF). We hypothesized that, in patients with chronic HF, Rho-kinase in circulating leukocytes is activated and related to left ventricular (LV) remodeling and dysfunction.
- ItemMitochondria, Myocardial Remodeling, and Cardiovascular Disease(2012) Verdejo, Hugo E.; del Campo, Andrea; Troncoso, Rodrigo; Gutierrez, Tomas; Toro, Barbra; Quiroga, Clara; Pedrozo, Zully; Pablo Munoz, Juan; Garcia, Lorena; Castro, Pablo F.; Lavandero, SergioThe process of muscle remodeling lies at the core of most cardiovascular diseases. Cardiac adaptation to pressure or volume overload is associated with a complex molecular change in cardiomyocytes which leads to anatomic remodeling of the heart muscle. Although adaptive at its beginnings, the sustained cardiac hypertrophic remodeling almost unavoidably ends in progressive muscle dysfunction, heart failure and ultimately death. One of the features of cardiac remodeling is a progressive impairment in mitochondrial function. The heart has the highest oxygen uptake in the human body and accordingly it has a large number of mitochondria, which form a complex network under constant remodeling in order to sustain the high metabolic rate of cardiac cells and serve as Ca2+ buffers acting together with the endoplasmic reticulum (ER). However, this high dependence on mitochondrial metabolism has its costs: when oxygen supply is threatened, high leak of electrons from the electron transport chain leads to oxidative stress and mitochondrial failure. These three aspects of mitochondrial function (Reactive oxygen species signaling, Ca2+ handling and mitochondrial dynamics) are critical for normal muscle homeostasis. In this article, we will review the latest evidence linking mitochondrial morphology and function with the process of myocardial remodeling and cardiovascular disease.
- ItemNew Molecular Insights of Insulin in Diabetic Cardiomyopathy(2016) Westermeier, Francisco; Riquelme, Jaime A.; Pavez, Mario; Garrido, Valeria; Diaz, Ariel; Verdejo Pinochet, Hugo; Castro Gálvez, Pablo Federico; Garcia, Lorena; Lavandero, Sergio
- ItemPolymorphisms in the RAC1 Gene Are Associated With Hypertension Risk Factors in a Chilean Pediatric Population(OXFORD UNIV PRESS, 2014) Tapia Castillo, Alejandra; Carvajal, Cristian A.; Campino, Carmen; Vecchiola, Andrea; Allende, Fidel; Solari, Sandra; Garcia, Lorena; Lavanderos, Sergio; Valdivia, Carolina; Fuentes, Cristobal; Lagos, Carlos F.; Martinez Aguayo, Alejandro; Baudrand, Rene; Aglony, Marlene; Garcia, Hernan; Fardella, Carlos E.The GTPase Rac1 has been implicated in hypertension as a modulator of mineralocorticoid receptor activity. Our aim is to investigate the frequency of polymorphisms rs10951982 (intron 1, G > A) and rs836478 (intron 3, T > C) in the RAC1 gene and perform association studies with clinical and biochemical parameters in a Chilean pediatric cohort.
- ItemRelationship between mechanical and metabolic dyssynchrony with left bundle branch block: Evaluation by 18-fluorodeoxyglucose positron emission tomography in patients with non-ischemic heart failure(ELSEVIER SCIENCE INC, 2012) Castro, Pablo; Luis Winter, Jose; Verdejo, Hugo; Orellana, Pilar; Carlos Quintana, Juan; Greig, Douglas; Enriquez, Andres; Sepulveda, Luis; Concepcion, Roberto; Sepúlveda Varela, Pablo Andrés; Rossel, Victor; Chiong, Mario; Garcia, Lorena; Lavandero, SergioBACKGROUND: Ventricular dyssynchrony is a common finding in patients with heart failure (HF), especially in the presence of conduction delays. The loss of ventricular synchrony leads to progressive impairment of contractile function, which may be explained in part by segmental abnormalities of myocardial metabolism. However, the association of these metabolic disarrangements with parameters of ventricular dyssynchrony and electrocardiography (ECG) findings has not yet been studied. METHODS: Our aim was to determine the correlation between the presence of left bundle branch block (LBBB) with left ventricular (LV) mechanical synchrony assessed by multiple-gated acquisition scan (MUGA) and with patterns of 18-fluorodeoxyglucose ((18)FDG) uptake in patients with non-ischemic heart failure. Twenty-two patients with non-ischemic cardiomyopathy, LV ejection fraction (LVEF) <= 45% and New York Heart Association (NYHA) Functional Class II or III symptoms under standard medical therapy were included, along with 10 healthy controls matched for age and gender. A 12-lead ECG was obtained to measure the length of the QRS. Mechanical LV synchrony was assessed by MUGA using phase analysis. All patients and controls underwent positron emission tomography with (18)FDG to determine the distribution of myocardial glucose uptake. The standard deviation of peak (18)FDG uptake was used as an index of metabolic heterogeneity. Student's t-test and Pearson's correlation were used for statistical analysis. RESULTS: The mean age of the patients with HF was 54 +/- 12 years and 72% were male. The length of the QRS was 129 +/- 31 milliseconds and LBBB was present in 9 patients. Patients with HF had decreased LV (18)FDG uptake compared with controls (7.56 +/- 3.36 vs 11.63 +/- 4.55 standard uptake value; p = 0.03). The length of the QRS interval correlated significantly with glucose uptake heterogeneity (r = 0.62; p = 0.002) and mechanical dyssynchrony (r = 0.63; p = 0.006). HF patients with LBBB showed marked glucose uptake heterogeneity compared with HF patients without LBBB (41.4 +/- 10 vs 34.7 +/- 4.9 ml/100 g/min, respectively; p = 0.01). CONCLUSIONS: Patients with non-ischemic heart failure exhibit a global decrease in myocardial glucose uptake. Within this group, subjects who also have LBBB exhibit a marked heterogeneity in segmental glucose uptake, which directly correlates with QRS duration. J Heart Lung Transplant 2012;31:1096-101 (C) 2012 International Society for Heart and Lung Transplantation. All rights reserved.
- ItemSoluble Interleukin-6 Receptor Regulates Interleukin-6-Dependent Vascular Remodeling in Long-Distance Runners(Frontiers Media S.A., 2021) Villar Fincheira, Paulina; Paredes, Aaron J.; Hernandez Diaz, Tomas; Norambuena Soto, Ignacio; Cancino Arenas, Nicole; Sanhueza Olivares, Fernanda; Contreras Briceño, Felipe; Mandiola Ovalle, Jorge; Bruneau, Nicole; Garcia, Lorena; Ocaranza, María Paz; Troncoso, Rodrigo; Gabrielli, Luigi; Chiong, MarioLittle is known about the effects of training load on exercise-induced plasma increase of interleukin-6 (IL-6) and soluble IL-6 receptor (sIL-6R) and their relationship with vascular remodeling. We sought to evaluate the role of sIL 6R as a regulator of IL-6-induced vascular remodeling. Forty-four male marathon runners were recruited and allocated into two groups: low-training (LT, <100 km/week) and high-training (HT, >= 100 km/week), 22 athletes per group. Twenty-one sedentary participants were used as reference. IL-6, sIL-6R and sgp130 levels were measured in plasma samples obtained before and immediately after finishing a marathon (42.2-km). Aortic diameter was measured by echocardiography. The inhibitory effect of sIL-6R on IL-6-induced VSMC migration was assessed using cultured A7r5 VSMCs. Basal plasma IL-6 and sIL-6R levels were similar among sedentary and athlete groups. Plasma IL-6 and sIL-6R levels were elevated after the marathon, and HT athletes had higher post-race plasma sIL-6R, but not IL-6, level than LT athletes. No changes in sgp130 plasma levels were found in LT and HT groups before and after running the marathon. Athletes had a more dilated ascending aorta and aortic root than sedentary participants with no differences between HT and LT athletes. However, a positive correlation between ascending aorta diameter and plasma IL-6 levels corrected by training load and years of training was observed. IL-6 could be responsible for aorta dilation because IL-6 stimulated VSMC migration in vitro, an effect that is inhibited by sIL-6R. However, IL-6 did not modify cell proliferation, collagen type I and contractile protein of VSMC. Our results suggest that exercise induces vascular remodeling. A possible association with IL-6 is proposed. Because sIL-6R inhibits IL-6-induced VSMC migration, a possible mechanism to regulate IL-6-dependent VSMC migration is also proposed.
- ItemXanthine-oxidase inhibitors and statins in chronic heart failure: Effects on vascular and functional parameters(ELSEVIER SCIENCE INC, 2011) Greig, Douglas; Alcaino, Hernan; Castro, Pablo F.; Garcia, Lorena; Verdejo, Hugo E.; Navarro, Mario; Lopez, Rafael; Mellado, Rosemarie; Tapia, Fabiola; Gabrielli, Luigi A.; Nogerol, Camilo; Chiong, Mario; Godoy, Ivan; Lavandero, SergioBACKGROUND: Increased oxidative stress in heart failure (HF) leads to inflammation and endothelial dysfunction (ED). Both statins and allopurinol have known anti-oxidant properties, but their utility in HF has not been fully assessed.