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dc.contributor.author
Ronda, Ana Carolina
dc.contributor.author
Vasconsuelo, Andrea Anahi
dc.contributor.author
Boland, Ricardo Leopoldo
dc.date.available
2018-12-12T16:00:37Z
dc.date.issued
2010-08
dc.identifier.citation
Ronda, Ana Carolina; Vasconsuelo, Andrea Anahi; Boland, Ricardo Leopoldo; Extracellular-regulated kinase and p38 mitogen-activated protein kinases are involved in the antiapoptotic action of 17β-estradiol in skeletal muscle cells; BioScientifica; Journal of Endocrinology; 206; 2; 8-2010; 235-246
dc.identifier.issn
0022-0795
dc.identifier.uri
http://hdl.handle.net/11336/66331
dc.description.abstract
17β-Estradiol (E2) stimulates the mitogen-activated protein kinases (MAPKs) in various cellular types.We have shown that the hormone activates extracellular-regulated kinase (ERK) and p38 MAPK in skeletal muscle cells. However, the functions of MAPK modulation by the estrogen in muscle cells have not been studied yet. We have recently reported antiapoptotic actions of E2 in C2C12 cells. Here, the role of MAPKs mediating the hormone effect in muscle cells was investigated. The results showed that cells exposed to 0.5 mM hydrogen peroxide (H2O2) presented cytoskeleton disorganization, mitochondrial redistribution, and picnotic/fragmented nuclei. Pretreatment with 10-8 M E2 prevented these morphological apoptotic characteristics, except in the presence of ERK or p38 MAPK inhibitors, U0126 and SB203580 respectively. Mitochondrial membrane integrity was also studied. Preincubation of cultures with 10-8 M E2 abrogated H2O2 effects such as Janus Green oxidation, presence of cytochrome c oxidase activity in the cytoplasm, and SMAC/DIABLO release from mitochondria. When MAPKs were inhibited, the hormone could not prevent mitochondrial membrane damage exerted by oxidative stress. Blocking experiments with small interfering RNAs confirmed that both ERK and p38 MAPKs mediate the antiapoptotic effects of the hormone at the mitochondrial level. Further, some of the molecular mechanisms involved were also investigated. Thus, E2 was able to induce AKT (Ser473) and BAD (Ser112) phosphorylation in C2C12 cells in the absence or in the presence of H2O2 but not when the cultures were incubated with H2O2 and MAPK inhibitors. Altogether, these results show that E2 exerts a survival action in skeletal muscle cells involving ERK and p38 MAPK activation. © 2010 Society for Endocrinology.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
BioScientifica
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Extracellular-Regulated Kinase
dc.subject.classification
Otras Ciencias Biológicas
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Ciencias Biológicas
dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
dc.title
Extracellular-regulated kinase and p38 mitogen-activated protein kinases are involved in the antiapoptotic action of 17β-estradiol in skeletal muscle cells
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-09-18T15:03:54Z
dc.identifier.eissn
1479-6805
dc.journal.volume
206
dc.journal.number
2
dc.journal.pagination
235-246
dc.journal.pais
Reino Unido
dc.journal.ciudad
Bristol
dc.description.fil
Fil: Ronda, Ana Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
dc.description.fil
Fil: Vasconsuelo, Andrea Anahi. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
dc.description.fil
Fil: 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; Argentina
dc.journal.title
Journal of Endocrinology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1677/JOE-09-0429
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://joe.bioscientifica.com/view/journals/joe/206/2/235.xml
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