Integrated analysis of the involvement of nitric oxide synthesis in mitochondrial proliferation, mitochondrial deficiency and apoptosis in skeletal muscle fibres

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dc.contributor.author Rodrigues, Gabriela Silva [UNIFESP]
dc.contributor.author Godinho, Rosely Oliveira [UNIFESP]
dc.contributor.author Kiyomoto, Beatriz Hitomi [UNIFESP]
dc.contributor.author Gamba, Juliana [UNIFESP]
dc.contributor.author Bulle Oliveira, Acary Souza [UNIFESP]
dc.contributor.author Schmidt, Beny [UNIFESP]
dc.contributor.author Tengan, Celia Harumi [UNIFESP]
dc.date.accessioned 2020-08-21T17:00:24Z
dc.date.available 2020-08-21T17:00:24Z
dc.date.issued 2016
dc.identifier http://dx.doi.org/10.1038/srep20780
dc.identifier.citation Scientific Reports. London, v. 6, p. -, 2016.
dc.identifier.issn 2045-2322
dc.identifier.uri https://repositorio.unifesp.br/handle/11600/57982
dc.description.abstract Nitric oxide (NO) is an important signaling messenger involved in different mitochondrial processes but only few studies explored the participation of NO in mitochondrial abnormalities found in patients with genetic mitochondrial deficiencies. In this study we verified whether NO synthase (NOS) activity was altered in different types of mitochondrial abnormalities and whether changes in mitochondrial function and NOS activity could be associated with the induction of apoptosis. We performed a quantitative and integrated analysis of NOS activity in individual muscle fibres of patients with mitochondrial diseases, considering mitochondrial function (cytochrome-c-oxidase activity), mitochondrial content, mitochondrial DNA mutation and presence of apoptotic nuclei. Our results indicated that sarcolemmal NOS activity was increased in muscle fibres with mitochondrial proliferation, supporting the relevance of neuronal NOS in the mitochondrial biogenesis process. Sarcoplasmic NOS activity was reduced in cytochrome-c-oxidase deficient fibres, probably as a consequence of the involvement of NO in the regulation of the respiratory chain. Alterations in NOS activity or mitochondrial abnormalities were not predisposing factors to apoptotic nuclei. Taken together, our results show that NO can be considered a potential molecular target for strategies to increase mitochondrial content and indicate that this approach may not be associated with increased apoptotic events. en
dc.description.sponsorship Sao Paulo Research Foundation (FAPESP)
dc.description.sponsorship Coordenacao de Aperfeicoamento de Pessoal de Ensino Superior (CAPES)
dc.format.extent -
dc.language.iso eng
dc.publisher Nature Publishing Group
dc.relation.ispartof Scientific Reports
dc.rights Acesso aberto
dc.title Integrated analysis of the involvement of nitric oxide synthesis in mitochondrial proliferation, mitochondrial deficiency and apoptosis in skeletal muscle fibres en
dc.type Artigo
dc.description.affiliation Univ Fed Sao Paulo, Escola Paulista Med, Dept Neurol & Neurosurg, Sao Paulo, Brazil
dc.description.affiliation Univ Fed Sao Paulo, Escola Paulista Med, Div Cellular Pharmacol, Sao Paulo, Brazil
dc.description.affiliation Univ Fed Sao Paulo, Escola Paulista Med, Dept Pathol, Sao Paulo, Brazil
dc.description.affiliationUnifesp Univ Fed Sao Paulo, Escola Paulista Med, Dept Neurol & Neurosurg, Sao Paulo, Brazil
dc.description.affiliationUnifesp Univ Fed Sao Paulo, Escola Paulista Med, Div Cellular Pharmacol, Sao Paulo, Brazil
dc.description.affiliationUnifesp Univ Fed Sao Paulo, Escola Paulista Med, Dept Pathol, Sao Paulo, Brazil
dc.description.sponsorshipID FAPESP: 2007/03145-9, 2007/00808-7
dc.identifier.file WOS000369617900001.pdf
dc.identifier.doi 10.1038/srep20780
dc.description.source Web of Science
dc.identifier.wos WOS:000369617900001
dc.coverage London
dc.citation.volume 6



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