Testosterone induces up-regulation of mitochondrial gene expression in murine C2C12 skeletal muscle cells accompanied by an increase of nuclear respiratory factor-1 and its downstream effectors

The reduction in muscle mass and strength with age, sarcopenia, is a prevalent condition among the elderly, linked to skeletal muscle dysfunction and cell apoptosis. We demonstrated that testosterone protects against H2O2-induced apoptosis in C2C12 muscle cells. Here, we analyzed the effect of testosterone on mitochondrial gene expression in C2C12 skeletal muscle cells. We found that testosterone increases mRNA expression of genes encoded by mitochondrial DNA, such as NADPH dehydrogenase subunit 1 (ND1), subunit 4 (ND4), cytochrome b (CytB), cytochrome c oxidase subunit 1 (Cox1) and subunit 2 (Cox2) in C2C12. Additionally, the hormone induced the expression of the nuclear respiratory factors 1 and 2 (Nrf-1 and Nrf-2), the mitochondrial transcription factors A (Tfam) and B2 (TFB2M), and the optic atrophy 1 (OPA1). The simultaneous treatment with testosterone and the androgen receptor antagonist, Flutamide, reduced these effects. H2O2-oxidative stress induced treatment, significantly decreased mitochondrial gene expression. Computational analysis revealed that mitochondrial DNA contains specific sequences, which the androgen receptor could recognize and bind, probably taking place a direct regulation of mitochondrial transcription by the receptor. These findings indicate that androgen plays an important role in the regulation of mitochondrial transcription and biogenesis in skeletal muscle.Fil: Pronsato, Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Milanesi, Lorena Magdalena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Vasconsuelo, Andrea Anahi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentin

Testosterone exerts antiapoptotic effects against H2O2 in C2C12 skeletal muscle cells through the apoptotic intrinsic pathway

Experimental data indicate that apoptosis is activated in the aged skeletal muscle, contributing to sarcopenia. We have previously demonstrated that testosterone protects against hydrogen peroxide (H2O2)-induced apoptosis in C2C12 muscle cells. Here we identified molecular events involved in the antiapoptotic effect of testosterone. At short times of exposure to H2O2 cells exhibit a defense response but at longer treatment times cells undergo apoptosis. Incubation with testosterone prior to H2O2 induces BAD inactivation, inhibition of poly (ADP-ribose) polymerase cleavage, and a decrease in BAX levels, and impedes the loss of mitochondrial membrane potential, suggesting that the hormone participates in the regulation of the apoptotic intrinsic pathway. Simultaneous treatment with testosterone, H2O2, and the androgen receptor (AR) antagonist, flutamide, reduces the effects of the hormone, pointing to a possible participation of the AR in the antiapoptotic effect. The data presented allow us to begin to elucidate the mechanism by which the hormone prevents apoptosis in skeletal muscle.Fil: Pronsato, Lucía. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; ArgentinaFil: Boland, Ricardo Leopoldo. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; ArgentinaFil: Milanesi, Lorena Magdalena. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; Argentin

Non-polar extracts of Nicotiana glauca (Solanaceae) induce apoptosis in human rhabdomyosarcoma cells

Rhabdomyosarcoma (RMS) is the most common soft-tissue tumour in children andadolescents. It originates in normal skeletal muscle from myogenic cells that have failed tofully differentiate, and it usually has a poor prognosis. Current RMS therapy has manyadverse effects. Hence, new treatments are needed. Various pharmacological properties,such as analgesic, antineoplastic, antimicrobial, and antiparasitic properties, have beendemonstrated in species of the Solanaceae family. We performed ethanolic extraction fromleaves of Nicotiana glauca (Solanaceae), and the extract was successively partitioned withn-hexane, chloroform, and ethyl acetate. We evaluated the effects of extracts on RMScells, and we found that the extracts trigger apoptosis. By bio-guided fractionation assays,we identified the apoptotic agents. Morphological assessment after apoptotic cell inductionof cultured cells, mitochondrial and nuclear morphology by Mitotracker, and 4,6-diamidino-2-phenylindole (DAPI) staining, respectively, were analysed in fluorescentmicroscopy. The capacity of the cells to migrate or proliferate was analysed by the Petitassay, followed by methylene blue staining. NMR and GC-MS spectrometry were used toidentify palmitic acid and scopoletin as the phytochemicals responsible for the observedeffects. These results indicate that these compounds are apoptotic inducers and they couldbe useful as chemotherapeutic agents against muscle tumours.Rabdomiossarcoma (RMS) é o tumor de tecidos moles mais comum em crianças e adolescentes. Ele se origina no músculo esquelético normal a partir de las células miogênicas que no conseguiram-se diferenciar completamente e pelo general tem um prognóstico ruim. A terapia atual com RMS tem muitos efeitos adversos e portanto, novos tratamentos são necessários. Várias propriedades farmacológicas, como propriedades analgésica, antineoplásica, antimicrobiana e antiparasitária, foram demostradas em espécies da família Solanaceae. Neste trabalho, foi realizada a extração etanólica das folhas de Nicotiana glauca (Solanaceae), eo extrato foi particionado sucessivamente com n-hexano, clorofórmio y acetato de etila. Avaliamos os efeitos dos extratos nas células RMS e descobrimos que os extratos desencadeiam apoptose. Pelos ensaios de fracionamento bio-guiado, identificamos os agentes apoptóticos. Avaliação morfológica após indução da apoptose das células cultivadas ea morfologia mitocondrial e nuclear por coloração com Mitotracker e 4,6-diamidino-2-fenilindol (DAPI), respectivamente, foram analisadas com microscopia fluorescente. A capacidade das células para migrar ou proliferar foi analisada hair ensaio Petit, seguido pelacoloração com azul de metileno. Una espectrometría de RMN y GC-MS para uso utilizado para una identificación de ácido palmítico y una escopoletina como fitoquímicos responsáveis ​​pelos efeitos observados.Fil: Musso, Florencia Antonella. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Química del Sur. Universidad Nacional del Sur. Departamento de Química. Instituto de Química del Sur; ArgentinaFil: Pronsato, Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Milanesi, Lorena Magdalena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Vasconsuelo, Andrea Anahi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Faraoni, María Belén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Química del Sur. Universidad Nacional del Sur. Departamento de Química. Instituto de Química del Sur; Argentin

High passage numbers induce resistance to apoptosis in C2C12 muscle cells

Cell lines with high passage numbers exhibit alterations in cell Morphology and functions. In the present work, C2C12 skeletal muscle cells with either low (60) passage numbers (identified as l-C2C12 or h-C2C12, respectively) were used to investigate the apoptotic response to H2O2 as a function of culture age h-C2C12. We found that older cultures (h-C2C12 group) were depleted of mitochondrial DNA (mtDNA). When we analyzed the behavior of Bad, Bax, caspase-3 and mitochondrial transmembrane potential, we observed that cells in the h-C2C12 group were resistant to H2O2 induction of apoptosis. We propose serially cultured C2C12 cells as a refractory model to H2O2-induced apoptosis. In addition, the data obtained in this work suggest that mtDNA is required for apoptotic cell death in skeletal muscle C2C12 cells.Fil: Pronsato, Lucía. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Bahia Blanca; Argentina;Fil: la Colla, Anabela Belén. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Laboratorio de Química Biológica; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Bahia Blanca; Argentina;Fil: Ronda, Ana Carolina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Cátedra de Química Biológica; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Bahia Blanca; Argentina;Fil: Milanesi, Lorena Magdalena. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Laboratorio de Química Biológica; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Bahia Blanca; Argentina;Fil: Boland, Ricardo Leopoldo. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Bahia Blanca; Argentina;Fil: Vasconsuelo, Andrea Anahi. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Laboratorio de Química Biológica; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Bahia Blanca; Argentina

El 17β-Estradiol y la Testosterona protegen a las mitocondrias contra el estrés oxidativo en Células del Músculo Esquelético

En trabajos previos demostramos que la testosterona (T) y el 17β-estradiol (E2) protegen a las células musculares C2C12 de la apoptosis inducida por peróxido de hidrógeno (H2O2). Conjuntamente evidenciamos la existencia de receptores de estrógenos y andrógenos en las mitocondrias. El presente trabajo se ha centrado en caracterizar los efectos de ambos esteroides en esta organela, que conducen a la supervivencia celular. Específicamente, se evaluaron las acciones de T y E2 sobre el potencial de membrana mitocondrial con el colorante JC-1 y sobre el poro de permeabilidad transitoria mitocondrial (MPTP) mediante el método de calcein-acetoxymethylester/cobalt, utilizando microscopía de fluorescencia y citometría de flujo. Demostramos que T y E2 previenen la apertura del MPTP y la pérdida de potencial de membrana mitocondrial inducidas por H2O2. Además, observamos que el H2O2 aumenta los niveles de expresión proteica del canal aniónico dependiente de voltaje (VDAC) e induce la translocación de Bax a mitocondria. Sin embargo, en presencia de las hormonas la translocación de Bax fue inhibida lo cual sugiere que los miembros de la familia Bcl -2 pueden ser regulados por E2 y T. Los eventos moleculares desencadenados por E2 y T a nivel mitocondrial se reflejaron en la morfología de las organelas. El análisis microscópico de las células C2C12 y cultivos primarios de músculo esquelético de ratón, mediante tinciones con verde de Jano y Mitotracker reveló un efecto protector de los esteroides contra el daño por estrés oxidativo inhibiendo la redistribución y picnosis mitocondrial.We have previously shown that testosterone (T) and 17β-estradiol (E2) protect C2C12 muscle cells against apoptosis induced by hydrogen peroxide (H2O2). Since we also showed the presence of estrogen and androgen Receptors in mitochondria, this work was focused on the effects of both steroids on this organelle, which result in cellular survival. Specifically, we evaluated the actions of T and E2 on the mitochondrial membrane potential with JC-1 dye and on the mitochondrial permeability transition pore (MPTP) by the calceinacetoxymethylester (AM)/cobalt method, using fluorescence microscopy and flow cytometry. We demonstrated that T and E2 prevent MPTP opening and the loss of mitochondrial membrane potential induced by H2O2. In addition, it was observed that H2O2 increase voltage-dependent anion channel (VDAC) protein expression levels and induce translocation of Bax to mitochondria. However, in the presence of the steroids Bax translocation was abrogated suggesting that members of the Bcl-2 family may be regulated by E2 and T. The observed effects triggered by E2 and T were reflected on mitochondrial morphology. Microscopic analysis of C2C12 cells and primary cultures of mouse skeletal muscle, with Janus Green and Mitotracker staining revealed a protective effect of the steroids against oxidative stress damage which included mitochondrial redistribution and pyknosis of the organelle.Fil: la Colla, Anabela Belén. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Pronsato, Lucía. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico Bahia Blanca. Instituto de Ciencias Biologicas y Biomedicas del Sur; ArgentinaFil: Ronda, Ana Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Bahía Blanca. Instituto Argentino de Oceanografía (i); Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Milanesi, Lorena Magdalena. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico Bahia Blanca. Instituto de Ciencias Biologicas y Biomedicas del Sur; ArgentinaFil: Vasconsuelo, Andrea Anahi. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico Bahia Blanca. Instituto de Ciencias Biologicas y Biomedicas del Sur; ArgentinaFil: Boland, Ricardo Leopoldo. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico Bahia Blanca. Instituto de Ciencias Biologicas y Biomedicas del Sur; Argentin

Subcellular Localization and Physiological Roles of Androgen Receptor

Androgens, such as testosterone and Dihydrotestosterone (DHT), exert theiractions through the Androgen Receptor (AR), a ligand-dependent nuclear transcription factor that belongs to the steroid hormone nuclear receptor superfamily. The actions of androgens can be mediated through the AR in a DNA binding-dependent manner to modulate the transcription of target genes, or in a manner independent of DNA binding, to trigger rapid cellular events such as the activation of the second messenger signaling pathway. The AR is expressed ubiquitously and it has a wide variety of biological actions comprising significant roles in the development and maintenance of the reproductive, skeletal muscle, cardiovascular, immune, neural and haemopoietic systems, exerting a diversity of roles in many physiological and pathological processes.Studies with AR Knockout (ARKO) mouse models, specifically the cell type- ortissue-specific ARKO models, have revealed many cell type- or tissue-specificpathophysiological roles of AR in mice. Because of the huge amount of nformationabout androgens and the AR, this chapter is not presented as an extensive review of all of it, but rather as an overview of the expression and biological Function of AR as well as its significant role in clinical medicine.Fil: Pronsato, Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentin

General Concepts of Skeletal Muscle and Apoptosis: Molecular Mechanisms and Regulation by Sex Steroids

Apoptosis is a physiologic process that take place during development andin the progression of specific diseases. In skeletal muscle, this process is poorly explored. Skeletal muscle represents an exceptional tissue regards apoptosis, by its multinucleated structure and its variable mitochondrial content. On the other hand, apoptosis of skeletal muscle tissue could have a wide spectrum of effects on organism since it is now well established that skeletal muscle not only generates force and movement; other functions are associated to this tissue. Skeletal muscle contributes to basal energy metabolism, in the storing for substrates such as amino acids and carbohydrates, in the keep of core temperature and blood glucose levels, and in the useof oxygen and energy during movement. Also, skeletal muscle acts as an endocrineorgan, thus could be regulated by owning or no own hormones. This chaptersummarizes the generalities of skeletal muscle at the molecular/structural and functional level and basic concepts of apoptosis, for a better understanding of the following chapters of this ebook. Which it focuses specifically, at a molecular level involving genomic regulation, on the actions of 17β-Estradiol and Testosterone in the homeostasis of skeletal muscle tissue in physiological and pathological conditions, converging in the relationship of muscle apoptosis and sexual hormones.Fil: Vasconsuelo, Andrea Anahi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Pronsato, Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentin

Role of testosterone in the intrinsic apoptotic pathway of skeletal muscle

Apoptosis is a systematic set of events that results in cellular self-destruction without inflammation or damage to the surrounding tissue. Experimental animal data indicate that apoptosis is activated in the aged skeletal muscle, contributing to the pathogenesis of sarcopenia. Given the role played by mitochondria in the induction and regulation of programmed cell death, intensive investigations have focused on mitochondria-driven myonuclear apoptosis. We have previously demonstrated that testosterone protects against H2O2-induced apoptosis in C2C12 muscle cells. Typical changes of apoptosis such as nuclear fragmentation, cytoskeleton disorganization, mitochondrial reorganization/dysfunction and cytochrome c release induced by H2O2, are abolished when cells are previously exposed to the hormone. In the present work, we identified molecular events that occur during the anti-apoptotic effect of testosterone on C2C12 cells. At short times of exposure to H2O2, cells exhibit a defense response showing ERK2, Akt and Bad phosphorylation and an increase of HSP70 levels. At longer treatment times with the apoptotic agent, dephosphorylation of the proteins mentioned before, cytochrome c release, PARP cleavage and DNA fragmentation occur, but when cells are treated with testosterone prior to H2O2, Bad inactivation (phosphorylation), an increase in actin levels, translocation of HSP90 to mitochondria and a decrease in Bax levels are observed, revealing that, the steroid hormone regulates the apoptotic intrinsic pathway. Although further studies are required to establish the molecular basis of sarcopenia associated to states of testosterone deficit, the data presented allow us to begin to elucidate the mechanism by which the hormone prevents apoptosis in skeletal muscle.Fil: Pronsato, Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Boland, Ricardo Leopoldo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Milanesi, Lorena Magdalena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentin

Non-classical localization of androgen binding proteins in the C2C12 skeletal muscle cell line

The classical model of testosterone action has been traditionally described as being mediated by the androgen receptor (AR) localized exclusively in the nucleus. However, there is increasing functional evidence for extranuclear localization of AR. We present biochemical and immunological data supporting mitochondrial and microsomal localization of AR in the C2C12 skeletal muscle cell line. As a first approach AR was detected by immunoblotting, using specific antibodies after subcellular fractionation, not only in nucleus and cytosol, but also in mitochondria and microsomes. We then established [3H] testosterone binding characteristics in total homogenates and subcellular fractions. Specific and saturable [3H] testosterone binding sites were detected in mitochondria and microsomes. Immunolocalization of the non-classical AR was also confirmed using confocal microscopy. Sucrose gradient fractionation demonstrated the presence of the AR in lipid rafts and caveolae. Besides, the AR interacts physically with Caveolin-1, association that is lost after testosterone treatment. Accordingly, Western blot analysis revealed a decrease of AR expression in the microsomal fraction after testosterone treatment, suggesting translocation of the membrane AR to another subcellular compartment. The non-classical distribution of native pools of AR in skeletal muscle cells suggests an alternative mode of AR localization/function.Fil: Pronsato, Lucía. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Bahia Blanca; ArgentinaFil: Boland, Ricardo Leopoldo. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Bahia Blanca; ArgentinaFil: Milanesi, Lorena Magdalena. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Bahia Blanca; Argentin

Role of androgen receptor in the protective action of testosterone during apoptosis in skeletal muscle

Fil: Pronsato, Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Boland, Ricardo Leopoldo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Milanesi, Lorena Magdalena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentin