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1.
Immunity ; 38(5): 1038-49, 2013 May 23.
Artículo en Inglés | MEDLINE | ID: mdl-23684988

RESUMEN

Macrophages act as the primary effector cells during Leishmania infection through production of reactive oxygen species (ROS) and interleukin-1ß (IL-1ß). However, how macrophage-killing mechanisms are activated during Leishmania-macrophage interactions is poorly understood. Here, we report that the macrophage response against Leishmania infantum in vivo is characterized by an M2b-like phenotype and C-type lectin receptors (CLRs) signature composed of Dectin-1, mannose receptor (MR), and the DC-SIGN homolog SIGNR3 expression. Dectin-1 and MR were crucial for the microbicidal response as indicated by the fact that they activated Syk-p47phox and arachidonic acid (AA)-NADPH oxidase signaling pathways, respectively, needed for ROS production and also triggered Syk-coupled signaling for caspase-1-induced IL-1ß secretion. In contrast, SIGNR3 has divergent functions during Leishmania infantum pathogenesis; this CLR favored parasite resilience through inhibition of the LTB4-IL-1ß axis. These pathways also operated during infection of primary human macrophages. Therefore, our study promotes CLRs as potential targets for treatment, diagnosis, and prevention of visceral leishmaniasis.


Asunto(s)
Antígenos CD/metabolismo , Lectinas Tipo C/metabolismo , Leishmania infantum/inmunología , Macrófagos/inmunología , Lectinas de Unión a Manosa/metabolismo , Receptores de Superficie Celular/metabolismo , Animales , Ácido Araquidónico/metabolismo , Caspasa 1/metabolismo , Células Cultivadas , Humanos , Interleucina-1beta/antagonistas & inhibidores , Interleucina-1beta/metabolismo , Péptidos y Proteínas de Señalización Intracelular/metabolismo , Lectinas Tipo C/inmunología , Leishmaniasis Visceral/inmunología , Leishmaniasis Visceral/parasitología , Leucotrieno B4/antagonistas & inhibidores , Receptor de Manosa , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , NADPH Oxidasas/metabolismo , Proteínas Tirosina Quinasas/metabolismo , Interferencia de ARN , ARN Interferente Pequeño , Especies Reactivas de Oxígeno/metabolismo , Transducción de Señal , Quinasa Syk
2.
Proc Natl Acad Sci U S A ; 114(4): E540-E549, 2017 01 24.
Artículo en Inglés | MEDLINE | ID: mdl-28069953

RESUMEN

Immune response against pathogens is a tightly regulated process that must ensure microbial control while preserving integrity of the infected organs. Tuberculosis (TB) is a paramount example of a chronic infection in which antimicrobial immunity is protective in the vast majority of infected individuals but can become detrimental if not finely tuned. Here, we report that C-type lectin dendritic cell (DC) immunoreceptor (DCIR), a key component in DC homeostasis, is required to modulate lung inflammation and bacterial burden in TB. DCIR is abundantly expressed in pulmonary lesions in Mycobacterium tuberculosis-infected nonhuman primates during both latent and active disease. In mice, we found that DCIR deficiency impairs STAT1-mediated type I IFN signaling in DCs, leading to increased production of IL-12 and increased differentiation of T lymphocytes toward Th1 during infection. As a consequence, DCIR-deficient mice control M. tuberculosis better than WT animals but also develop more inflammation characterized by an increased production of TNF and inducible NOS (iNOS) in the lungs. Altogether, our results reveal a pathway by which a C-type lectin modulates the equilibrium between infection-driven inflammation and pathogen's control through sustaining type I IFN signaling in DCs.


Asunto(s)
Células Dendríticas/inmunología , Interferón Tipo I/inmunología , Lectinas Tipo C/inmunología , Tuberculosis/inmunología , Animales , Femenino , Lectinas Tipo C/genética , Macaca mulatta , Ratones Endogámicos C57BL , Ratones Noqueados , Fosforilación , Factor de Transcripción STAT1/inmunología , Transducción de Señal
3.
Immunol Cell Biol ; 92(8): 699-708, 2014 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-24890643

RESUMEN

Mononuclear phagocytes (MP) comprise monocytes, macrophages (MΦ) and dendritic cells (DC), including their lineage-committed progenitors, which together have an eminent role in health and disease. Lipid-based siRNA-mediated gene inactivation is an established approach to investigate gene function in MP cells. However, although there are few protocols dedicated for siRNA-mediated gene inactivation in primary human DC and MΦ, there are none available for primary human monocytes. Moreover, there is no available method to perform comparative studies of a siRNA-mediated gene silencing in primary monocytes and other MP cells. Here, we describe a protocol optimized for the lipid-based delivery of siRNA to perform gene silencing in primary human blood monocytes, which is applicable to DCs, and differs from the classical route of siRNA delivery into MΦs. Along with this protocol, we provide a comparative analysis of how monocytes, DC and MΦ are efficiently transfected with the target siRNA without affecting cell viability, resulting in strong gene knockdown efficiency, including the simultaneous inactivation of two genes. Moreover, siRNA delivery does not affect classical functions in MP such as differentiation, phagocytosis and migration, demonstrating that this protocol does not induce non-specific major alterations in these cells. As a proof-of-principle, a functional analysis of hematopoietic cell kinase (Hck) shows for the first time that this kinase regulates the protease-dependent migration mode in human monocytes. Collectively, this protocol enables efficient gene inactivation in primary MP, suggesting a wide spectrum of applications such as siRNA-based high-throughput screening, which could ultimately improve our knowledge about MP biology.


Asunto(s)
Células Dendríticas/metabolismo , Silenciador del Gen , Macrófagos/metabolismo , Monocitos/metabolismo , ARN Interferente Pequeño/genética , Animales , Diferenciación Celular/genética , Movimiento Celular/genética , Movimiento Celular/inmunología , Células Dendríticas/citología , Células Dendríticas/inmunología , Expresión Génica , Técnicas de Silenciamiento del Gen , Humanos , Macrófagos/citología , Macrófagos/inmunología , Ratones , Ratones Noqueados , Monocitos/citología , Monocitos/inmunología , Fagocitosis/inmunología , Proteínas Proto-Oncogénicas c-hck/genética , Proteínas Proto-Oncogénicas c-hck/metabolismo , Interferencia de ARN , ARN Mensajero/genética , Transfección
4.
Br J Nutr ; 112(5): 674-87, 2014 Sep 14.
Artículo en Inglés | MEDLINE | ID: mdl-24949706

RESUMEN

As the understanding of the nutritional regulation of muscle growth mechanisms in fish is fragmentary, the present study aimed to (1) characterise ontogenetic changes in muscle growth-related genes in parallel to changes in muscle cellularity; (2) determine whether an early decrease in dietary protein:energy ratio by fat addition affects the muscle growth mechanisms of rainbow trout (Oncorhynchus mykiss) alevins; and (3) determine whether this early feeding of a high-fat (HF) diet to alevins had a long-term effect on muscle growth processes in juveniles fed a commercial diet. Developmental regulation of hyperplasia and hypertrophy was evidenced at the molecular (expression of myogenic regulatory factors, proliferating cell nuclear antigen and myosin heavy chains (MHC)) and cellular (number and diameter of white muscle fibres) levels. An early decrease in dietary protein:energy ratio by fat addition stimulated the body growth of alevins but led to a fatty phenotype, with accumulation of lipids in the anterior part, and less caudal muscle when compared at similar body weights, due to a decrease in both the white muscle hyperplasia and maximum hypertrophy of white muscle fibres. These HF diet-induced cellular changes were preceded by a very rapid down-regulation of the expression of fast-MHC. The present study also demonstrated that early dietary composition had a long-term effect on the subsequent muscle growth processes of juveniles fed a commercial diet for 3 months. When compared at similar body weights, initially HF diet-fed juveniles indeed had a lower mean diameter of white muscle fibres, a smaller number of large white muscle fibres, and lower expression levels of MyoD1 and myogenin. These findings demonstrated the strong effect of early feed composition on the muscle growth mechanisms of trout alevins and juveniles.


Asunto(s)
Grasas de la Dieta/administración & dosificación , Proteínas en la Dieta/administración & dosificación , Ingestión de Energía , Desarrollo de Músculos , Músculo Esquelético/crecimiento & desarrollo , Oncorhynchus mykiss/crecimiento & desarrollo , Fenómenos Fisiológicos Nutricionales de los Animales , Animales , Dieta/veterinaria , Hiperplasia , Hipertrofia , Lípidos/análisis , Fibras Musculares de Contracción Rápida/patología , Proteína MioD/genética , Miogenina/genética , Cadenas Pesadas de Miosina/genética , Antígeno Nuclear de Célula en Proliferación/genética
5.
Hum Mol Genet ; 17(12): 1762-73, 2008 Jun 15.
Artículo en Inglés | MEDLINE | ID: mdl-18344354

RESUMEN

X-linked adrenoleukodystrophy (X-ALD) is a fatal neurodegenerative disorder, characterized by progressive cerebral demyelination cerebral childhood adrenoleukodystrophy (CCALD) or spinal cord neurodegeneration (adrenomyeloneuropathy, AMN), adrenal insufficiency and accumulation of very long-chain fatty acids (VLCFA) in tissues. The disease is caused by mutations in the ABCD1 gene, which encodes a peroxisomal transporter that plays a role in the import of VLCFA or VLCFA-CoA into peroxisomes. The Abcd1 knockout mice develop a spinal cord disease that mimics AMN in adult patients, with late onset at 20 months of age. The mechanisms underlying cerebral demyelination or axonal degeneration in spinal cord are unknown. Here, we present evidence by gas chromatography/mass spectrometry that malonaldehyde-lysine, a consequence of lipoxidative damage to proteins, accumulates in the spinal cord of Abcd1 knockout mice as early as 3.5 months of age. At 12 months, Abcd1- mice accumulate additional proteins modified by oxidative damage arising from metal-catalyzed oxidation and glycoxidation/lipoxidation. While we show that VLCFA excess activates enzymatic antioxidant defenses at the protein expression levels, both in neural tissue, in ex vivo organotypic spinal cord slices from Abcd1- mice, and in human ALD fibroblasts, we also demonstrate that the loss of Abcd1 gene function hampers oxidative stress homeostasis. We find that the alpha-tocopherol analog Trolox is able to reverse oxidative lesions in vitro, thus providing therapeutic hope. These results pave the way for the identification of therapeutic targets that could reverse the deregulated response to oxidative stress in X-ALD.


Asunto(s)
Adrenoleucodistrofia/metabolismo , Oxidación-Reducción , Médula Espinal/metabolismo , Animales , Catalasa/metabolismo , Quimiocina CCL22/genética , Quimiocina CCL22/metabolismo , Cromanos/farmacología , Ácidos Grasos/metabolismo , Fibroblastos/metabolismo , Humanos , Técnicas In Vitro , Lisina/metabolismo , Malondialdehído/metabolismo , Potencial de la Membrana Mitocondrial/efectos de los fármacos , Ratones , Ratones Endogámicos C57BL , Neuronas Motoras/enzimología , Neuronas Motoras/metabolismo , Estrés Oxidativo , Superóxido Dismutasa
6.
Front Immunol ; 9: 1123, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29946317

RESUMEN

DC-SIGN (CD209/CLEC4L) is a C-type lectin receptor (CLR) that serves as a reliable cell-surface marker of interleukin 4 (IL-4)-activated human macrophages [M(IL-4)], which historically represent the most studied subset within the M2 spectrum of macrophage activation. Although DC-SIGN plays important roles in Mycobacterium tuberculosis (Mtb) interactions with dendritic cells, its contribution to the Mtb-macrophage interaction remains poorly understood. Since high levels of IL-4 are correlated with tuberculosis (TB) susceptibility and progression, we investigated the role of DC-SIGN in M(IL-4) macrophages in the TB context. First, we demonstrate that DC-SIGN expression is present both in CD68+ macrophages found in tuberculous pulmonary lesions of non-human primates, and in the CD14+ cell population isolated from pleural effusions obtained from TB patients (TB-PE). Likewise, we show that DC-SIGN expression is accentuated in M(IL-4) macrophages derived from peripheral blood CD14+ monocytes isolated from TB patients, or in macrophages stimulated with acellular TB-PE, arguing for the pertinence of DC-SIGN-expressing macrophages in TB. Second, using a siRNA-mediated gene silencing approach, we performed a transcriptomic analysis of DC-SIGN-depleted M(IL-4) macrophages and revealed the upregulation of pro-inflammatory signals in response to challenge with Mtb, as compared to control cells. This pro-inflammatory gene signature was confirmed by RT-qPCR, cytokine/chemokine-based protein array, and ELISA analyses. We also found that inactivation of DC-SIGN renders M(IL-4) macrophages less permissive to Mtb intracellular growth compared to control cells, despite the equal level of bacteria uptake. Last, at the molecular level, we show that DC-SIGN interferes negatively with the pro-inflammatory response and control of Mtb intracellular growth mediated by another CLR, Dectin-1 (CLEC7A). Collectively, this study highlights a dual role for DC-SIGN as, on the one hand, being a host factor granting advantage for Mtb to parasitize macrophages and, on the other hand, representing a molecular switch to turn off the pro-inflammatory response in these cells to prevent potential immunopathology associated to TB.


Asunto(s)
Moléculas de Adhesión Celular/metabolismo , Lectinas Tipo C/metabolismo , Macrófagos/inmunología , Macrófagos/metabolismo , Mycobacterium tuberculosis/inmunología , Receptores de Superficie Celular/metabolismo , Tuberculosis/inmunología , Tuberculosis/metabolismo , Animales , Moléculas de Adhesión Celular/genética , Supervivencia Celular/genética , Supervivencia Celular/inmunología , Citocinas/metabolismo , Femenino , Expresión Génica , Interacciones Huésped-Patógeno/genética , Interacciones Huésped-Patógeno/inmunología , Humanos , Mediadores de Inflamación/metabolismo , Lectinas Tipo C/genética , Macaca mulatta , Macrófagos/microbiología , Monocitos/inmunología , Monocitos/metabolismo , Fagocitosis/inmunología , Receptores de Superficie Celular/genética , Tuberculosis/genética , Tuberculosis/microbiología
7.
Int J Biochem Cell Biol ; 39(1): 146-60, 2007.
Artículo en Inglés | MEDLINE | ID: mdl-16968671

RESUMEN

While the acquisition of apoptosis resistance is part of the differentiation program of skeletal muscle cells, differentiated muscle cells can undergo apoptosis in response to physiological or pathological stimuli. The generation of reactive oxygen species by mitochondria plays a major role in the control of apoptosis in many cell types. Indeed their involvement in controlling apoptosis in differentiated muscle cells, or in generating resistance to apoptosis remains unknown. Moreover, differentiated muscle cells specifically express the uncoupling protein-3, a mitochondrial protein potentially involved in controlling reactive oxygen species production. To study the role of mitochondrial reactive oxygen species in the control of apoptosis in skeletal muscle cells, L6E9 myoblasts and myotubes were exposed to staurosporine, an inducer of apoptosis via mitochondrial pathways. Staurosporine activated apoptotic pathways (i.e. caspase-3 and caspase-9) increasing reactive oxygen species in myoblasts and, to a minor extent, in myotubes. However, the increase in reactive oxygen species was not needed to induce apoptosis nor was it involved in the differential sensitization of myoblasts and myotubes to apoptosis. Moreover, expression of uncoupling protein-3 in myotubes did not affect reactive oxygen species production, although it produced a slight sensitization for staurosporine-induced apoptosis. Results indicate that apoptotic activation in skeletal muscle cells mainly involves reactive oxygen species-independent mechanisms and that mitochondrial uncoupling protein-3 is not protective either for reactive oxygen species production or for apoptotic activation in muscle cells.


Asunto(s)
Apoptosis/fisiología , Canales Iónicos/metabolismo , Mitocondrias Musculares/metabolismo , Proteínas Mitocondriales/metabolismo , Fibras Musculares Esqueléticas/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Animales , Apoptosis/efectos de los fármacos , Caspasa 3/metabolismo , Caspasa 9/metabolismo , Línea Celular , Inhibidores Enzimáticos/farmacología , Fibras Musculares Esqueléticas/citología , Músculo Esquelético/citología , Músculo Esquelético/metabolismo , Ratas , Estaurosporina/farmacología , Proteína Desacopladora 3
8.
FEBS Lett ; 581(5): 955-61, 2007 Mar 06.
Artículo en Inglés | MEDLINE | ID: mdl-17303124

RESUMEN

Fatty acids induced an increase in reactive oxygen species (ROS) and enhanced NF-kappaB activation in L6 myotubes differentiated in culture. Palmitate proved more effective than oleate in eliciting these effects. The induction of uncoupling protein-3 (UCP3) at levels similar to those occurring in vivo, attained through the use of an adenoviral vector, led to a reduction of mitochondrial membrane potential in L6 myotubes. However, the capacity of palmitate to increase ROS was not reduced but, quite the opposite, it was moderately enhanced due to the presence of UCP3. The presence of UCP3 in mitochondria did not modify the expression of genes encoding ROS-related enzymes, either in basal conditions or in the presence of palmitate. However, in the presence of UCP3, UCP2 mRNA expression was down-regulated in response to palmitate. We conclude that UCP3 does not act as a protective agent against palmitate-dependent induction of ROS production in differentiated skeletal muscle cells.


Asunto(s)
Canales Iónicos/metabolismo , Proteínas Mitocondriales/metabolismo , Fibras Musculares Esqueléticas/efectos de los fármacos , Fibras Musculares Esqueléticas/metabolismo , Ácido Palmítico/farmacología , Animales , Línea Celular , Expresión Génica , Canales Iónicos/genética , Potencial de la Membrana Mitocondrial , Mitocondrias/metabolismo , Proteínas Mitocondriales/genética , Ácido Oléico/farmacología , Ratas , Especies Reactivas de Oxígeno/metabolismo , Proteínas Recombinantes/genética , Proteínas Recombinantes/metabolismo , Transducción Genética , Proteína Desacopladora 2 , Proteína Desacopladora 3
9.
PLoS One ; 10(7): e0132692, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26173080

RESUMEN

Understanding the molecular components of immune recognition of the tuberculosis (TB) bacillus, Mycobacterium tuberculosis, can help designing novel strategies to combat TB. Here, we identify collectin CL-LK as a novel soluble C-type lectin able to bind M. tuberculosis, and characterize mycobacterial mannose-capped lipoarabinomannan as a primary ligand for CL-LK. Mice deficient in CL-K1, one of the CL-LK subunits, do not display altered susceptibility to M. tuberculosis. However, we found that the amount of CL-LK in the serum of patients with active TB is reduced, compared to that in controls, and correlates inversely to the magnitude of the immune response to the pathogen. These findings indicate that CL-LK might be of interest for future diagnostic and treatment monitoring purposes.


Asunto(s)
Colectinas/inmunología , Mycobacterium tuberculosis/inmunología , Receptores de Reconocimiento de Patrones/metabolismo , Animales , Estudios de Casos y Controles , Colectinas/sangre , Colectinas/deficiencia , Colectinas/genética , Femenino , Humanos , Técnicas In Vitro , Ligandos , Lipopolisacáridos/inmunología , Lipopolisacáridos/metabolismo , Ratones , Ratones Endogámicos C57BL , Ratones Noqueados , Mycobacterium tuberculosis/patogenicidad , Tuberculosis Pulmonar/sangre , Tuberculosis Pulmonar/inmunología
10.
Free Radic Biol Med ; 35(12): 1589-98, 2003 Dec 15.
Artículo en Inglés | MEDLINE | ID: mdl-14680682

RESUMEN

Cell proliferation of vascular cells is a key feature in vascular biology, wound healing, and pathophysiological processes such as atherosclerosis and restenosis. In atherosclerotic intima, cell proliferation colocalizes with oxidized LDL that indicate a local oxidative stress. This study aims to investigate whether cell proliferation is causally related with extracellular ROS generation and subsequent LDL oxidation. Sparse proliferating endothelial and smooth muscle cells generate higher levels of extracellular ROS (O2*- and H2O2) and LDL oxidation than confluent contact-inhibited cells. During wound healing of confluent cell layer, cell proliferation associated with healing also induced enhanced extracellular ROS generation and LDL oxidation. Proliferation-associated extracellular ROS generation is mediated through mitogenic signaling pathways, involving ERK1/2 and PKC, but is independent of de novo DNA synthesis, gene expression and protein synthesis. Data obtained with inhibitors of oxidases suggest that proliferation-associated extracellular ROS are not generated by a single ROS-generating system and are not essential for cell proliferation. In conclusion, our data show that proliferating vascular cells (in sparse culture or during wound healing) generate high levels of extracellular ROS and LDL oxidation through regulation of ROS-generating systems by mitogenic signaling. This constitutes a link between proliferative events and oxidative stress/LDL oxidation in atherosclerotic lesions and restenosis.


Asunto(s)
División Celular/fisiología , Lipoproteínas LDL/metabolismo , Especies Reactivas de Oxígeno , Cicatrización de Heridas/fisiología , Animales , Endotelio Vascular/citología , Endotelio Vascular/enzimología , Endotelio Vascular/metabolismo , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos , Proteínas Quinasas Activadas por Mitógenos/metabolismo , Oxidación-Reducción , Proteína Quinasa C/metabolismo , Conejos
12.
Biochem Cell Biol ; 80(6): 757-64, 2002.
Artículo en Inglés | MEDLINE | ID: mdl-12555808

RESUMEN

Uncoupling protein 2 (UCP-2) belongs to the mitochondrial anion carrier family. It is ubiquitously expressed but is most abdundant in the reticuloendothelial system. In addition to uncoupling function, UCP-2 modulates the production of reactive oxygen species (ROS) by isolated mitochondria. Using an antisense oligonucleotide strategy, we investigated whether a defect in UCP-2 expression modulates ROS in intact endothelial cells. Murine endothelial cells (CRL 2181) pretreated by antisense oligonucleotides directed against UCP-2 mRNA exhibited a significant and specific increase in membrane potential and intracellular ROS level compared with control scrambled or anti-UCP-1 and -UCP-3 antisense oligonucleotides. These specific changes induced by UCP-2 antisense oligonucleotides were correlated with a rise in extracellular superoxide anion production and oxidative stress assessed by thiobarbituric acid reactive substance values. Taken together, these data suggest a role for UCP-2 in control of ROS production and subsequent oxidation of surrounding compounds mediating oxidative stress of endothelial cells. These data also support the notion that manipulations of UCP-2 at the genetic level could control ROS metabolism at the cellular level.


Asunto(s)
Endotelio/metabolismo , Proteínas de Transporte de Membrana , Proteínas Mitocondriales , Oligonucleótidos Antisentido/metabolismo , Proteínas/genética , Proteínas/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Animales , Línea Celular , Regulación hacia Abajo , Endotelio/citología , Canales Iónicos , Ratones , Oligonucleótidos Antisentido/genética , Oxidación-Reducción , ARN Mensajero/genética , ARN Mensajero/metabolismo , Rodamina 123 , Sustancias Reactivas al Ácido Tiobarbitúrico/análisis , Proteína Desacopladora 2
13.
Biochem J ; 367(Pt 3): 889-94, 2002 Nov 01.
Artículo en Inglés | MEDLINE | ID: mdl-12153397

RESUMEN

Mitochondria generate reactive oxygen species (ROS) under various pathophysiological conditions. In isolated mitochondria, fatty acids (FA) exhibit an uncoupling effect of the respiratory activity and modulate ROS generation. The effect of FA on intact cultured cells remains to be elucidated. The present study reports that FA (buffered by BSA) decrease the level of cellular ROS generated by the mitochondrial respiratory chain in cultured cells incubated with antimycin A. Both saturated and unsaturated FA are effective. This fatty acid-induced antioxidant effect does not result from a decrease in ROS production, but is subsequent to cellular glutathione peroxidase (GPx) activation and enhanced ROS degradation. This fatty acid-induced GPx activation is mediated through epidermal growth factor receptor (EGFR) signalling, since this response is (i) abrogated by the EGFR inhibitor AG1478 or by a defect in EGFR (in EGFR-deficient B82L fibroblasts), (ii) restored in B82LK+ cells expressing EGFR and (iii) mimicked by epidermal growth factor. These findings indicate that FA contribute to enhance cellular antioxidant defences against mitochondrial oxidative stress through EGFR-dependent GPx activation.


Asunto(s)
Receptores ErbB/fisiología , Glutatión Peroxidasa/metabolismo , Mitocondrias/efectos de los fármacos , Ácido Oléico/farmacología , Estrés Oxidativo , Línea Celular , Activación Enzimática , Humanos , Mitocondrias/metabolismo , Especies Reactivas de Oxígeno/metabolismo
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