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1. Subcellular distribution of ERK phosphorylation in tyrosine and threonine depends on redox status in murine lung cells.

Author

Katia E Helfenberger, Nerina M Villalba, Bruno Buchholz, Alberto Boveris, Juan José Poderoso, Ricardo J Gelpi, and Cecilia Poderoso

Subjects
Medicine, Science
Abstract

Activation of ERK1/2 implies the phosphorylation of tyrosine (pTyr) and threonine (pThr) by MEK1/2; both reactions were thought to be cytoplasmic, promoting ERK to reach the nucleus where it activates several transcription factors. In addition, H2O2 concentrations are known to modulate ERK intracellular translocation, which impacts on cellular proliferation. In this context, the objective of this work was to study the sequence of ERK phosphorylation under two redox conditions and to analyze a putative mitochondrial contribution to this process, in LP07 murine lung cells. A time-course of H2O2 administration was used and ERK phosphorylation was analyzed in cytosol, mitochondria and nuclei. At 1μM H2O2, a proliferative redox stimulus, immunoblot revealed a fast and transient increase in cytosol pTyr and a sustained increase in mitochondrial pTyr content. The detection for pThr/pTyrERK (2pERK) showed in cytosol a marked increase at 5 minutes with a fast dephosphorylation after that time, for both H2O2 concentrations. However, at 50 μM H2O2, an anti-proliferative condition, 2pERK was gradually retained in mitochondria. Interestingly, these results were confirmed by in vivo experiments using mice treated with a highly oxidizing agent [H2O2]. By the use of two ERK2 mutant constructions, where Tyr and Thr were replaced by alanine, we confirmed that 2pERK relied almost completely on pThr183. Confocal microscopy confirmed ERK subcellular distribution dependence on the incidence of cytosolic pTyr and mitochondrial pThr at 1μM H2O2. This work shows for the first time, both in vitro and in vivo, an ERK cycle involving a cross-talk between cytosol and mitochondria phosphorylation events, which may play a significant role in cell cycle progression, proliferation or differentiation under two different redox conditions.

Published
2018
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2. Pilocarpine-Induced Status Epilepticus Is Associated with P-Glycoprotein Induction in Cardiomyocytes, Electrocardiographic Changes, and Sudden Death

Author

Jerónimo Auzmendi, Bruno Buchholz, Jimena Salguero, Carlos Cañellas, Jazmín Kelly, Paula Men, Marcela Zubillaga, Alicia Rossi, Amalia Merelli, Ricardo J. Gelpi, Alberto J. Ramos, and Alberto Lazarowski

Subjects
Status Epilepticus, SUDEP, HIF-1α, hypoxia, P-glycoprotein, cardiomyocytes, QT prolongation, Medicine, Pharmacy and materia medica, RS1-441
Abstract

Sudden unexpected death in epilepsy (SUDEP) is the major cause of death in those patients suffering from refractory epilepsy (RE), with a 24-fold higher risk relative to the normal population. SUDEP risk increases with seizure frequency and/or seizure-duration as in RE and Status Epilepticus (SE). P-glycoprotein (P-gp), the product of the multidrug resistant ABCB1-MDR-1 gene, is a detoxifying pump that extrudes drugs out of the cells and can confer pharmacoresistance to the expressing cells. Neurons and cardiomyocytes normally do not express P-gp, however, it is overexpressed in the brain of patients or in experimental models of RE and SE. P-gp was also detected after brain or cardiac hypoxia. We have previously demonstrated that repetitive pentylenetetrazole (PTZ)-induced seizures increase P-gp expression in the brain, which is associated with membrane depolarization in the hippocampus, and in the heart, which is associated with fatal SE. SE can produce hypoxic-ischemic altered cardiac rhythm (HIACR) and severe arrhythmias, and both are related with SUDEP. Here, we investigate whether SE induces the expression of hypoxia-inducible transcription factor (HIF)-1α and P-gp in cardiomyocytes, which is associated with altered heart rhythm, and if these changes are related with the spontaneous death rate. SE was induced in Wistar rats once a week for 3 weeks, by lithium-pilocarpine-paradigm. Electrocardiograms, HIF-1α, and P-gp expression in cardiomyocytes, were evaluated in basal conditions and 72 h after SE. All spontaneous deaths occurred 48 h after each SE was registered. We observed that repeated SE induced HIF-1α and P-gp expression in cardiomyocytes, electrocardiographic (ECG) changes, and a high rate of spontaneous death. Our results suggest that the highly accumulated burden of convulsive stress results in a hypoxic heart insult, where P-gp expression may play a depolarizing role in cardiomyocyte membranes and in the development of the ECG changes, such as QT interval prolongation, that could be related with SUDEP. We postulate that this mechanism could explain, in part, the higher SUDEP risk in patients with RE or SE.

Published
2018
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3. Chronic exposure to urban air pollution in Buenos Aires city induces oxidative stress, inflammation and olfactory alteration over time in mice olfactory bulb

Author

Agustina L. Freire, Mariana S. Garcés, Sofía Reynoso, Lourdes C. Cáceres, Octavio Diana, Timoteo O. Marchini, Nahuel Mendez Diodiati, Manuela Martinefski, Valeria Tripodi, Jorge Goldstein, Bruno Buchholz, Silvia Alvarez, Natalia D. Magnani, and Pablo Evelson

Subjects
Physiology (medical), Biochemistry
Published
2023
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6. Chronic exposure to polluted urban air aggravates myocardial infarction by impaired cardiac mitochondrial function and dynamics

Author

Timoteo Marchini, Natalia Magnani, Mariana Garces, Jazmin Kelly, Mariela Paz, Lourdes Caceres, Valeria Calabro, Romina Lasagni Vitar, Laura Caltana, Mario Contin, Sofia Reynoso, Nestor Lago, Tamara Vico, Virginia Vanasco, Dennis Wolf, Valeria Tripodi, Daniel Gonzalez Maglio, Silvia Alvarez, Bruno Buchholz, Alejandro Berra, Ricardo Gelpi, and Pablo Evelson

Subjects
Mice, Air Pollution, Health, Toxicology and Mutagenesis, Myocardial Infarction, Animals, Particulate Matter, Hydrogen Peroxide, General Medicine, Toxicology, Pollution, Mitochondria
Abstract

Air pollution exposure positively correlates with increased cardiovascular morbidity and mortality rates, mainly due to myocardial infarction (MI). Herein, we aimed to study the metabolic mechanisms underlying this association, focusing on the evaluation of cardiac mitochondrial function and dynamics, together with its impact over MI progression. An initial time course study was performed in BALB/c mice breathing filtered air (FA) or urban air (UA) in whole-body exposure chambers located in Buenos Aires City downtown for up to 16 weeks (n = 8 per group and time point). After 12 weeks, lung inflammatory cell recruitment was evident in UA-exposed mice. Interestingly, impaired redox metabolism, characterized by decreased lung SOD activity and increased GSSG levels and NOX activity, precede local inflammation in this group. At this selected time point, additional mice were exposed to FA or UA (n = 12 per group) and alveolar macrophage PM uptake and nitric oxide (NO) production was observed in UA-exposed mice, together with increased pro-inflammatory cytokine levels (TNF-α and IL-6) in BAL and plasma. Consequently, impaired heart tissue oxygen metabolism and altered mitochondrial ultrastructure and function were observed in UA-exposed mice after 12 weeks, characterized by decreased active state respiration and ATP production rates, and enhanced mitochondrial H

Published
2022
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7. Vagal stimulation mimics preconditioning and postconditioning of ischemic myocardium in mice by activating different protection mechanisms

Author

Marina C. Muñoz, Fernando P. Dominici, Daniel Horacio Gonzalez Maglio, Eduardo Alberto Bernatene, Nahuel Méndez Diodati, Ricardo J. Gelpi, Bruno Buchholz, and Jazmín Kelly

Subjects
Male, 0301 basic medicine, Time Factors, CIENCIAS MÉDICAS Y DE LA SALUD, Vagal stimulation, Vagus Nerve Stimulation, alpha7 Nicotinic Acetylcholine Receptor, Physiology, Ischemic myocardium, Myocardial Infarction, Ischemia, Myocardial Reperfusion Injury, 030204 cardiovascular system & hematology, Pharmacology, Mice, 03 medical and health sciences, 0302 clinical medicine, α7 nicotinic acetylcholine receptor, Physiology (medical), Muscarinic acetylcholine receptor, medicine, Animals, Ischemic Postconditioning, Cholinergic anti-inflammatory pathway, Glycogen Synthase Kinase 3 beta, business.industry, Myocardium, Heart, Vagus Nerve, Α7-NICOTINIC ACETYLCHOLINE RECEPTOR, Patología, Janus Kinase 2, medicine.disease, Receptors, Muscarinic, MYOCARDIAL ISCHEMIA-REPERFUSION, CHOLINERGIC ANTI-INFLAMMATORY PATHWAY, Disease Models, Animal, Medicina Básica, 030104 developmental biology, MUSCARINIC RECEPTOR, VAGAL NERVE STIMULATION, Ischemic Preconditioning, Myocardial, Cytokines, Cardiology and Cardiovascular Medicine, business, Proto-Oncogene Proteins c-akt, Signal Transduction
Abstract

Vagal stimulation (VS) during myocardial ischemia and reperfusion has beneficial effects. However, it is not known whether short-term VS applied before ischemia or at the onset of reperfusion protects the ischemic myocardium. This study was designed to determine whether short-term VS applied before ischemia or at the onset of reperfusion reduces myocardial infarct size (IS), mimicking classic preconditioning and postconditioning. A second objective was to study the participation of muscarinic and nicotinic receptors in the protection of both preischemic and reperfusion stimulation. FVB mice were subjected to 30 min of regional myocardial ischemia followed by 2 h of reperfusion without VS, with 10-min preischemic VS (pVS), or with VS during the first 10 min of reperfusion (rVS). pVS reduced IS, and this effect was abolished by atropine and wortmannin. rVS also reduced IS in a similar manner, and this effect was abolished by the α7-nicotinic acetylcholine receptor blocker methyllycaconitine. pVS increased Akt and glycogen synthase kinase (GSK)-3β phosphorylation. No changes in Akt and GSK-3β phosphorylation were observed in rVS. Stimulation-mediated IS protection was abolished with the JAK2 blocker AG490. rVS did not modify IL-6 and IL-10 levels in the plasma or myocardium. Splenic denervation and splenectomy did not abolish the protective effect of rVS. In conclusion, pVS and rVS reduced IS by different mechanisms: pVS activated the Akt/GSK-3β muscarinic pathway, whereas rVS activated α7-nicotinic acetylcholine receptors and JAK2, independently of the cholinergic anti-inflammatory pathway. NEW & NOTEWORTHY Our data suggest, for the first time, that vagal stimulation applied briefly either before ischemia or at the beginning of reperfusion mimics classic preconditioning and postconditioning and reduces myocardial infarction, activating different mechanisms. We also infer an important role of α7-nicotinic receptors for myocardial protection independent of the cholinergic anti-inflammatory pathway. Fil: Buchholz, Bruno. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina Fil: Kelly, Jazmín. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Muñoz, Marina Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Bernatene, Eduardo Alberto. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Méndez Diodati, Nahuel. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina Fil: Gonzalez Maglio, Daniel Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni; Argentina Fil: Dominici, Fernando Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina Fil: Gelpi, Ricardo Jorge. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; Argentina

Published
2018
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9. Impaired lung redox metabolism and cardiac mitochondrial function aggravates myocardial infarction in a mice model of chronic exposure to urban air pollution

Author

Virginia Vanasco, Mario Contin, Tamara Vico, Silvia Alvarez, Ricardo J. Gelpi, Timoteo Marchini, Romina Mayra Lasagni Vitar, Valeria Calabró, Daniel Horacio Gonzalez Maglio, Valeria Tripodi, Laura Caltana, Sofía Reynoso, Néstor Lago, Natalia Magnani, Pablo Evelson, Mariela L. Paz, Lourdes Cáceres, Mariana Garcés, Bruno Buchholz, Kelly Jazmín, and Alejandro Berra

Subjects
Chronic exposure, medicine.medical_specialty, Lung, business.industry, medicine.disease, Biochemistry, Redox metabolism, medicine.anatomical_structure, Physiology (medical), Internal medicine, medicine, Cardiology, Myocardial infarction, business, Function (biology)
Published
2021
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15. Rosuvastatin Given During Reperfusion Decreases Infarct Size and Inhibits Matrix Metalloproteinase-2 Activity in Normocholesterolemic and Hypercholesterolemic Rabbits

Author

Lukas Erni, Regina Wikinski, Cristina Lorenzo Carrión, Nidia Basso, Bruno Buchholz, Laura Schreier, Martín Donato, Gabriela Berg, Verónica D'Annunzio, Verónica Miksztowicz, and Ricardo J. Gelpi

Subjects
medicine.medical_specialty, CIENCIAS MÉDICAS Y DE LA SALUD, MATRIX METALLOPROTEINASES, Matrix metalloproteinase inhibitor, Hypercholesterolemia, Myocardial Infarction, Ischemia, Myocardial Reperfusion, Myocardial Reperfusion Injury, Medicina Clínica, Matrix Metalloproteinase Inhibitors, Pharmacology, Matrix metalloproteinase, Internal medicine, medicine, STATINS, Animals, Rosuvastatin, cardiovascular diseases, Myocardial infarction, Rosuvastatin Calcium, Doxycycline, Cardioprotection, Sulfonamides, Sistemas Cardíaco y Cardiovascular, business.industry, MYOCARDIAL INFARCTION, Myocardium, nutritional and metabolic diseases, medicine.disease, Fluorobenzenes, Pyrimidines, Cardiology, Matrix Metalloproteinase 2, Rabbits, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Cardiology and Cardiovascular Medicine, business, Reperfusion injury, medicine.drug
Abstract

There is evidence that statin treatment before ischemia protects myocardium from ischemia/reperfusion injury. Objective: to determine whether rosuvastatin administered during reperfusion modifies infarct size and the recovery of postischemic ventricular dysfunction in normo and hypercholesterolemic rabbit. Additionally, we also evaluated the role of MMP-2 activation. Langendorff-perfused rabbit hearts were subjected to 30 minutes of ischemia and 120 minutes of reperfusion. In group 2, we added rosuvastatin after 30 minutes of ischemia and from the beginning of reperfusion. In group 3, an MMP inhibitor (doxycycline) was administered during the first 2 min of reperfusion. Finally, we repeated these groups but in hypercholesterolemic rabbits (Groups 4, 5 and 6). The infarct size was 16.6±2.6% in group 1 and 25.6±2.7% in group 4. Rosuvastatin reduced infarct size to 4.5±1.1% and 5.5±1.6% in groups 2 and 5, respectively (p

Published
2009
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16. Complex I syndrome in myocardial stunning and the effect of adenosine

Author

Laura B. Valdez, Alberto Boveris, Martín Donato, Darío E. Iglesias, Ricardo J. Gelpi, Silvina Sonia Bombicino, Verónica D'Annunzio, Bruno Buchholz, and Tamara Zaobornyj

Subjects
Adenosine, Mitochondrion, Protein oxidation, Biochemistry, Mitochondria, Heart, MYOCARDIAL ISCHEMIA/REPERFUSION, chemistry.chemical_compound, MITOCHONDRIA, FREE RADICALS, Heart metabolism, Myocardial Stunning, biology, ADENOSINE, PEROXYNITRITE, Nitric oxide synthase, Mitochondrial matrix, Reperfusion Injury, Rabbits, COMPLEX I, NITRIC OXIDE, CIENCIAS NATURALES Y EXACTAS, MYOCARDIAL STUNNING, medicine.drug, NITROTYROSINE, medicine.medical_specialty, Otras Ciencias Biológicas, Heart Ventricles, Cell Respiration, TBARS, Nitric oxide, MTNOS, Ciencias Biológicas, Oxygen Consumption, Physiology (medical), Internal medicine, medicine, MN-SOD, Animals, Myocardial stunning, Electron Transport Complex I, Superoxide Dismutase, PROTEIN CARBONYLS, medicine.disease, Disease Models, Animal, Endocrinology, chemistry, biology.protein, Lipid Peroxidation, Nitric Oxide Synthase
Abstract

Isolated rabbit hearts were exposed to ischemia (I; 15 min) and reperfusion (R; 5-30 min) in a model of stunned myocardium. I/R decreased left-ventricle O 2 consumption (46%) and malate-glutamate-supported mitochondrial state 3 respiration (32%). Activity of complex I was 28% lower after I/R. The pattern observed for the decline in complex I activity was also observed for the reduction in mitochondrial nitric oxide synthase (mtNOS) biochemical (28%) and functional (50%) activities, in accordance with the reported physical and functional interactions between complex I and mtNOS. Malate-glutamate-supported state 4 H 2O 2 production was increased by 78% after I/R. Rabbit heart Mn-SOD concentration in the mitochondrial matrix (7.4 ± 0.7 μM) was not modified by I/R. Mitochondrial phospholipid oxidation products were increased by 42%, whereas protein oxidation was only slightly increased. I/R produced a marked (70%) enhancement in tyrosine nitration of the mitochondrial proteins. Adenosine attenuated postischemic ventricular dysfunction and protected the heart from the declines in O 2 consumption and in complex I and mtNOS activities and from the enhancement of mitochondrial phospholipid oxidation. Rabbit myocardial stunning is associated with a condition of dysfunctional mitochondria named "complex I syndrome." The beneficial effect of adenosine could be attributed to a better regulation of intracellular cardiomyocyte Ca 2+ concentration. © 2011 Elsevier Inc. Fil: Valdez, Laura Batriz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Zaobornyj, Tamara. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Bombicino, Silvina Sonia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Iglesias, Dario Ezequiel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Boveris, Alberto Antonio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica; Argentina Fil: Donato, Pablo Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina Fil: D'Anunzio, Verónica. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina Fil: Buchholz, Bruno. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina Fil: Gelpi, Ricardo Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina

Published
2011

17. Über den Jodgehalt menschlicher Organe

Author

Bruno Buchholz

Subjects
Gynecology, medicine.medical_specialty, Philosophy, medicine, General Medicine
Abstract

Aus den vorliegenden Versuchen ergibt sich: 1. Alle Gewebe im menschlichen Korper sind jodhaltig. Ein konstanter Organjodspiegel existiert jedoch nicht. 2. Das Jod der Schilddruse betragt ungefahr 1/6–1/7 des Gesamtkorperjods. 3. Auch in anderen innersekretorischen Drusen, vor allem in Nebenniere und Ovar, findet sich konstant ein uber dem sonstigen Korperjod piegender Wert. 4. Eine gewisse Konstanz im prozentualen Jodgehalt findet sich nur bei der Schilddruse, nicht bei anderen Organen. 5. Im Gebiete aktiver Entzundungen findet eine Anreicherung an Jod statt. 6. Zwischen der Funktion eines innersekretorischen Organs und seinem Jodgehalt scheint eine Abhangigkeit zu bestehen. Der Nachweis hierfur ist am Eierstock gelungen. Der in voller Funktion befindliche Eierstock der Frau hat einen Jodgehalt von im Durchschnitt 90 γ-%, nach der Menopause ist kaum noch Jod nachweisbar (etwa 10 γ-%). 7. In welcher Form das Jod in den einzelnen Korperteilen vorliegt, ist vorlaufig nicht zu entscheiden. Es ist fur die innersekretorischen Organe daran zu denken, das es hier als Schilddrusenhormon vorkommt. Deshalb ist durch vorliegende Untersuchungen keineswegs die Schilddruse als dominierendes Organ des Jodstoffwechsels entsetzt.

Published
1928
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18. Der Komplementschwund im Blute

Author

W. H. Veil and Bruno Buchholz

Subjects
Genetics, business.industry, Drug Discovery, Molecular Medicine, Medicine, General Medicine, business, Molecular medicine, Genetics (clinical), Human genetics
Published
1932
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