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7 results on '"Mitocondrias"'

1. Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions

Author

Apostolova, Nadezda, Iannantuoni, Francesca, Gruevska, Aleksandra, Muntane, Jordi, Rocha, Milagros, Victor, Victor M., Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (España), Instituto de Salud Carlos III, European Commission, Generalitat Valenciana, Ministerio de Ciencia, Innovación y Universidades (España), Agencia Estatal de Investigación (España), Junta de Andalucía, Grupo Menarini, Fundación Juan Esplugues, [Apostolova,N, Gruevska,A] Department of Pharmacology, University of Valencia – FISABIO (Foundation for the Promotion of Health and Biomedical Research in the Valencian Region), Valencia, Spain. [Apostolova,N, Rocha,M, Victor,VM] CIBERehd (Biomedical Research Networking Centre on Hepatic and Digestive Diseases), Valencia, Spain. [Iannantuoni,F, Victor,VM] Service of Endocrinology and Nutrition. University Hospital Doctor Peset, FISABIO, Valencia, Spain. [Muntane,J] Institute of Biomedicine of Seville (IBiS), University Hospital 'Virgen del Rocío'/CSIC/University of Seville, Seville, Spain. [Victor,VM] Department of Physiology, University of Valencia, Valencia, Spain., This work was funded by grants PI16/00090, PI19/00838, PI19/0437,PI19/01266 and CIBERehd CB06/04/0071 by Carlos III Health Institute and by the European Regional Development Fund (ERDF ‘‘A way to build Europe’‘), by PROMETEO/2019/027 by Ministry of Education of the Valencian Regional Government, and by RTI2018-096748-B-100 (Spanish Ministry of Science, Innovation and Universities), by Andalusian Ministry of Economy, Innovation, Science and Employment (CTS-6264), Andalusian Ministry of Equality, Health and Social Policies (PI-0198-2016) and by an unrestricted grant from Menarini S.A. M.R and VM.V are recipients of contracts from the Ministry of Health of the Valencian Regional Government and Carlos III Health Institute (CPII16/00037 and CES10/030, respectively) while AG is supported by the Foundation 'Juan Esplugues'.

Subjects
Terapéutica, Analytical, Diagnostic and Therapeutic Techniques and Equipment::Therapeutics [Medical Subject Headings], Diseases::Endocrine System Diseases::Diabetes Mellitus::Diabetes Mellitus, Type 2 [Medical Subject Headings], Estrés oxidativo, Type 2 diabetes, Fisiología, Atherosclerosis, Pathophysiology, Metformin, Mitochondria, Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings], Treatment, Phenomena and Processes::Physiological Phenomena::Physiological Processes::Stress, Physiological::Oxidative Stress [Medical Subject Headings], Diabetes mellitus tipo 2, Diseases::Cardiovascular Diseases::Vascular Diseases::Arterial Occlusive Diseases::Arteriosclerosis::Atherosclerosis [Medical Subject Headings], Anatomy::Cells::Blood Cells::Leukocytes [Medical Subject Headings], Oxidative stress, Anatomy::Tissues::Epithelium::Endothelium [Medical Subject Headings], Chemicals and Drugs::Organic Chemicals::Amidines::Guanidines::Biguanides::Metformin [Medical Subject Headings], Metformina, Mitocondrias, Aterosclerosis, Anatomy::Cells::Cellular Structures::Intracellular Space::Cytoplasm::Cytoplasmic Structures::Organelles::Mitochondria [Medical Subject Headings]
Abstract

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin is still not fully understood. This review provides an overview of the existing literature concerning the beneficial mitochondrial and vascular effects of metformin, which it exerts by diminishing oxidative stress and reducing leukocyte-endothelium interactions. Specifically, we describe the molecular mechanisms involved in metformin's effect on gluconeogenesis, its capacity to interfere with major metabolic pathways (AMPK and mTORC1), its action on mitochondria and its antioxidant effects. We also discuss potential targets for therapeutic intervention based on these molecular actions. This work was funded by grants PI16/00090, PI19/00838, PI19/0437,PI19/01266 and CIBERehd CB06/04/0071 by Carlos III Health Institute and by the European Regional Development Fund (ERDF ‘‘A way to build Europe’‘); by PROMETEO/2019/027 by Ministry of Education of the Valencian Regional Government; by RTI2018-096748-B-100 (Spanish Ministry of Science, Innovation and Universities), by Andalusian Ministry of Economy, Innovation, Science and Employment (CTS-6264), Andalusian Ministry of Equality, Health and Social Policies (PI-0198-2016) and by an unrestricted grant from Menarini S.A. M.R and VM.V are recipients of contracts from the Ministry of Health of the Valencian Regional Government and Carlos III Health Institute (CPII16/00037 and CES10/030, respectively) while AG is supported by the Foundation “Juan Esplugues”.

Published
2020

2. High density lipoproteins selectively promote the survival of human regulatory T cells

Author

Courtney M. Jackson, W. Sean Davidson, Maria E. Moreno-Fernandez, Ana Lucia Rodríguez-Perea, Cesar M. Rueda, Claire A. Chougnet, and John T. Melchior

Subjects
0301 basic medicine, lymphocytes, Regulatory T cell, T cell, Immunology, Inmunología, chemical and pharmacologic phenomena, QD415-436, Mitochondrion, Biochemistry, Lipids/oxidation, immunology, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, medicine, Lymphocytes, Scavenger receptor, Receptor, Mitocondrias, Chemistry, Linfocitos, hemic and immune systems, Cell Biology, lipids/oxidation, Cell biology, Mitochondria, mitochondria, 030104 developmental biology, medicine.anatomical_structure, Apoptosis, 030220 oncology & carcinogenesis, lipids (amino acids, peptides, and proteins), Energy source, Homeostasis
Abstract

HDLs appear to affect regulatory T cell (Treg) homeostasis, as suggested by the increased Treg counts in HDL-treated mice and by the positive correlation between Treg frequency and HDL-cholesterol levels in statin-treated healthy adults. However, the underlying mechanisms remain unclear. Herein, we show that HDLs, not LDLs, significantly decreased the apoptosis of human Tregs in vitro, whereas they did not alter naïve or memory CD4+T cell survival. Sim- ilarly, oleic acid bound to serum albumin increased Treg sur- vival. Tregs bound and internalized high amounts of HDL compared with other subsets, which might arise from the higher expression of the scavenger receptor class B type I by Tregs; accordingly, blocking this receptor hindered HDL- mediated Treg survival. Mechanistically, we showed that HDL increased Treg ATP concentration and mitochondrial activity, enhancing basal respiration, maximal respiration, and spare respiratory capacity. Blockade of FA oxidation by etoxomir abolished the HDL-mediated enhanced survival and mitochondrial activity. Our findings thus suggest that Tregs can specifically internalize HDLs from their microenvironment and use them as an energy source. Furthermore, a novel implication of our data is that enhanced Treg survival may contribute to HDLs’ anti-inflammatory properties. COL0012444

Published
2017

3. In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2 + cross talk and loss of store-operated Ca2 + entry (SOCE) in rat hippocampal neurons

Author

Maria Calvo-Rodriguez, Lucía Núñez, Carlos Villalobos, Mónica García-Durillo, Junta de Castilla y León, Ministerio de Economía y Competitividad (España), and European Commission

Subjects
0301 basic medicine, Orai1, Aging, Envejecimiento, Biology, 03 medical and health sciences, Cognitive decline, Uniporter, Molecular Biology, Mitocondrias, Calcium signaling, ER-mitochondria cross talking, Endoplasmic reticulum, STIM1, Store-operated calcium entry, Cell Biology, Anatomy, Retículo endoplasmático, Cell biology, Mitochondria, 030104 developmental biology, Stim1, Neuronas hipocampales, Hippocampal neurons, Neuron death, Cell aging
Abstract

Producción Científica, Aging is associated to cognitive decline and susceptibility to neuron death, two processes related recently to subcellular Ca2+ homeostasis. Memory storage relies on mushroom spines stability that depends on store-operated Ca2 + entry (SOCE). In addition, Ca2+ transfer from endoplasmic reticulum (ER) to mitochondria sustains energy production but mitochondrial Ca2+ overload promotes apoptosis. We have addressed whether SOCE and ER-mitochondria Ca2+ transfer are influenced by culture time in long-term cultures of rat hippocampal neurons, a model of neuronal aging. We found that short-term cultured neurons show large SOCE, low Ca2+ store content and no functional coupling between ER and mitochondria. In contrast, in long-term cultures reflecting aging neurons, SOCE is essentially lost, Stim1 and Orai1 are downregulated, Ca2+ stores become overloaded, Ca2+ release is enhanced, expression of the mitochondrial Ca2+ uniporter (MCU) increases and most Ca2 + released from the ER is transferred to mitochondria. These results suggest that neuronal aging is associated to increased ER-mitochondrial cross talking and loss of SOCE. This subcellular Ca2+ remodeling might contribute to cognitive decline and susceptibility to neuron cell death in the elderly., Ministerio de Economía, Industria y Competitividad (grants BFU2012-37146 and BFU2015-70131R), Junta de Castilla y León (grants VA145U13 and BIO/VA33/13)

Published
2016

4. In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2 + cross talk and loss of store-operated Ca2 + entry (SOCE) in rat hippocampal neurons

Author

Calvo Rodríguez, María and Calvo Rodríguez, María

Abstract

Producción Científica, Aging is associated to cognitive decline and susceptibility to neuron death, two processes related recently to subcellular Ca2+ homeostasis. Memory storage relies on mushroom spines stability that depends on store-operated Ca2 + entry (SOCE). In addition, Ca2+ transfer from endoplasmic reticulum (ER) to mitochondria sustains energy production but mitochondrial Ca2+ overload promotes apoptosis. We have addressed whether SOCE and ER-mitochondria Ca2+ transfer are influenced by culture time in long-term cultures of rat hippocampal neurons, a model of neuronal aging. We found that short-term cultured neurons show large SOCE, low Ca2+ store content and no functional coupling between ER and mitochondria. In contrast, in long-term cultures reflecting aging neurons, SOCE is essentially lost, Stim1 and Orai1 are downregulated, Ca2+ stores become overloaded, Ca2+ release is enhanced, expression of the mitochondrial Ca2+ uniporter (MCU) increases and most Ca2 + released from the ER is transferred to mitochondria. These results suggest that neuronal aging is associated to increased ER-mitochondrial cross talking and loss of SOCE. This subcellular Ca2+ remodeling might contribute to cognitive decline and susceptibility to neuron cell death in the elderly., Ministerio de Economía, Industria y Competitividad (grants BFU2012-37146 and BFU2015-70131R), Junta de Castilla y León (grants VA145U13 and BIO/VA33/13)

Published
2016

5. The expression of the mitochondrial encoded gene ND4 is downregulated in cystic fibrosis

Author

Valdivieso, Ángel Gabriel, Marcucci, Florencia, Taminelli, Guillermo, González Guerrico, Anatilde, Alvarez, Sergio, Dankert, Marcelo A., Teiber, María Luz, and Santa Coloma, Tomás Antonio

Subjects
GLIBURIDA, MT-ND4, MITOCONDRIAS, CFTR(inh)-172, FIBROSIS QUISTICA, CFTR, CFDE, GENES MITOCONDRIALES
Abstract

Fil: Valdivieso, Ángel G. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: Valdivieso, Ángel G. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: Valdivieso, Ángel G. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Valdivieso, Ángel G. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Fil: Marcucci, Florencia. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: Marcucci, Florencia. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: Marcucci, Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Marcucci, Florencia. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Fil: Taminelli, Guillermo. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: Taminelli, Guillermo. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: Taminelli, Guillermo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Taminelli, Guillermo. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Fil: González Guerrico, Anatilde. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: González Guerrico, Anatilde. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: González Guerrico, Anatilde. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: González Guerrico, Anatilde. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Fil: Alvarez, Sergio. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: Alvarez, Sergio. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: Alvarez, Sergio. Consejo Nacional de Investigaciones Científicas; Argentina Fil: Alvarez, Sergio. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Fil: Dankert, Marcelo A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: Dankert, Marcelo A. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: Dankert, Marcelo A. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Dankert, Marcelo A. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Fil: Teiber, María Luz. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: Teiber, María Luz. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: Teiber, María Luz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Teiber, María Luz. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Fil: Santa Coloma, Tomás A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina Fil: Santa Coloma, Tomás A. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas; Argentina Fil: Santa Coloma, Tomás A. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Santa Coloma, Tomás A. Universidad Católica Argentina. Facultad de Ciencias Médicas. Programa de Investigaciones Biomédicas; Argentina Abstract: Cystic fibrosis (CF) is a disease produced by mutations in the CFTR channel. We have previously reported that the CFTR chloride transport activity regulates the differential expression of several genes, including SRC. Here we report that MT-ND4, a mitochondrial gene encoding a subunit of the mitochondrial Complex I (mtCx-I), is also a CFTR-dependent gene. A reduced expression of MT-ND4 was observed in CFDE cells (derived from a CF patient) when compared to CFDE cells ectopically expressing wild type CFTR. The differential expression of MT-ND4 in CF was confirmed by PCR. In situ hybridizations of deparaffinized human lung tissue slices derived from wt-CFTR or CF patients also showed downregulation of ND4 in CF. In addition, glibenclamide or CFTR(inh)-172 (CFTR chloride transport inhibitors) reduced MT-ND4 expression in cells expressing wt CFTR. These results suggest that the CFTR chloride transport activity indirectly up-regulates MT-ND4 expression.

Published
2007

6. Nonsteroidal anti-inflammatory drugs inhibit vascular smooth muscle cell proliferation by enabling the Ca2+-dependent inactivation of calcium release-activated calcium/Orai channels normally prevented by mitocondria

Author

Muñoz Conejero, Eva and Muñoz Conejero, Eva

Abstract

Producción Científica, Abnormal vascular smooth muscle cell (VSMC) proliferation contributes to occlusive and proliferative disorders of the vessel wall. Salicylate and other nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit VSMC proliferation by an unknown mechanism unrelated to anti-inflammatory activity. In search for this mechanism, we have studied the effects of salicylate and other NSAIDs on subcellular Ca2+ homeostasis and Ca2+-dependent cell proliferation in rat aortic A10 cells, a model of neointimal VSMCs. We found that A10 cells displayed both store-operated Ca2+ entry (SOCE) and voltage-operated Ca2+ entry (VOCE), the former being more important quantitatively than the latter. Inhibition of SOCE by specific Ca2+ released-activated Ca2+ (CRAC/Orai) channels antagonists prevented A10 cell proliferation. Salicylate and other NSAIDs, including ibuprofen, indomethacin, and sulindac, inhibited SOCE and thereby Ca2+-dependent, A10 cell proliferation. SOCE, but not VOCE, induced mitochondrial Ca2+ uptake in A10 cells, and mitochondrial depolarization prevented SOCE, thus suggesting that mitochondrial Ca2+ uptake controls SOCE (but not VOCE) in A10 cells. NSAIDs depolarized mitochondria and prevented mitochondrial Ca2+ uptake, suggesting that they favor the Ca2+-dependent inactivation of CRAC/Orai channels. NSAIDs also inhibited SOCE in rat basophilic leukemia cells where mitochondrial control of CRAC/Orai is well established. NSAIDs accelerate slow inactivation of CRAC currents in rat basophilic leukemia cells under weak Ca2+ buffering conditions but not in strong Ca2+ buffer, thus excluding that NSAIDs inhibit SOCE directly. Taken together, our results indicate that NSAIDs inhibit VSMC proliferation by facilitating the Ca2+-dependent inactivation of CRAC/Orai channels which normally is prevented by mitochondria clearing of entering Ca2+., Junta de Castilla y León (grants SAN191/VA1806 and CSI12A08), Ministerio de Ciencia, Innovación y Universidades (grant BFU2009-0867), Deutsche Forschungsgemeinschaft (grant A3)

Published
2011

7. Mitochondrial [Ca2+] oscillations driven by local high [Ca2+] domains generated by spontaneous electric activity

Author

Villalobos Jorge, Carlos and Villalobos Jorge, Carlos

Abstract

Producción Científica, Mitochondria take up calcium during cell activation thus shaping Ca2+ signaling and exocytosis. In turn, Ca2+ uptake by mitochondria increases respiration and ATP synthesis. Targeted aequorins are excellent Ca2+ probes for subcellular analysis, but single-cell imaging has proven difficult. Here we combine virus-based expression of targeted aequorins with photon-counting imaging to resolve dynamics of the cytosolic, mitochondrial, and nuclear Ca2+ signals at the single-cell level in anterior pituitary cells. These cells exhibit spontaneous electric activity and cytosolic Ca2+oscillations that are responsible for basal secretion of pituitary hormones and are modulated by hypophysiotrophic factors. Aequorin reported spontaneous [Ca2+] oscillations in all the three compartments, bulk cytosol, nucleus, and mitochondria. Interestingly, a fraction of mitochondria underwent much larger [Ca2+] oscillations, which were driven by local high [Ca2+] domains generated by the spontaneous electric activity. These oscillations were large enough to stimulate respiration, providing the basis for local tune-up of mitochondrial function by the Ca2+ signal., Dirección General de Enseñanza Superior (grants PB97-0474, APC1999-011 and 1FD97-1725-C02-02)

Published
2001

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