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dc.contributor.author
Peixoto, Estanislao  
dc.contributor.author
Atorrasagasti, María Catalina  
dc.contributor.author
Malvicini, Mariana  
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Fiore, Esteban Juan  
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Rodriguez, Marcelo  
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García, Mariana Gabriela  
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Finocchieto, Paola  
dc.contributor.author
Poderoso, Juan José  
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Corrales, Fernando  
dc.contributor.author
Mazzolini Rizzo, Guillermo Daniel  
dc.date.available
2018-05-11T17:23:50Z  
dc.date.issued
2016-05  
dc.identifier.citation
Peixoto, Estanislao; Atorrasagasti, María Catalina; Malvicini, Mariana; Fiore, Esteban Juan; Rodriguez, Marcelo; et al.; SPARC gene deletion protects against toxic liver injury and is associated to an enhanced proliferative capacity and reduced oxidative stress response; Impact Journals; Oncotarget; 5-2016; 1-11  
dc.identifier.issn
1949-2553  
dc.identifier.uri
http://hdl.handle.net/11336/44928  
dc.description.abstract
SPARC, also known as osteonectin and BM-40, is a matricellular protein with a number of biological functions. Hepatic SPARC expression is induced in response to thioacetamide, bile-duct ligation, and acute injuries such as concanavalin A and lipopolysacharide (LPS)/D-galactosamine. We have previously demonstrated that the therapeutic inhibition of SPARC or SPARC gene deletion protected mice against liver injury. We investigated the mechanisms involved in the protective effect of SPARC inhibition in mice. We performed a proteome analysis of livers from SPARC+/+ and SPARC−/− mice chronically treated with thioacetamide. Catalase activity, carbonylation levels, oxidative stress response, and mitochondrial function were studied. Genomic analysis revealed that SPARC−/− mice had an increased expression of cell proliferation genes. Proteins involved in detoxification of reactive oxygen species such as catalase, peroxirredoxine-1, and glutathione-S-transferase P1 and Mu1 were highly expressed as evidenced by proteome analysis; hepatic catalase activity was increased in SPARC−/− mice. Oxidative stress response and carbonylation levels were lower in livers from SPARC−/− mice. Hepatic mitochondria showed lower levels of nitrogen reactive species in the SPARC−/− concanavalin A-treated mice. Mitochondrial morphology was preserved, and its complex activity reduced in SPARC−/− mice. In conclusion, our data suggest that the protection associated with SPARC gene deletion may be partially due to a higher proliferative capacity of hepatocytes and an enhanced oxidative stress defense in SPARC−/− mice after liver injury.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
Impact Journals  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
Sparc  
dc.subject
Hepatocyte Proliferation  
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Liver Damage  
dc.subject.classification
Bioquímica y Biología Molecular  
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Medicina Básica  
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CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
SPARC gene deletion protects against toxic liver injury and is associated to an enhanced proliferative capacity and reduced oxidative stress response  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2018-03-27T15:17:17Z  
dc.journal.pagination
1-11  
dc.journal.pais
Estados Unidos  
dc.journal.ciudad
Albany  
dc.description.fil
Fil: Peixoto, Estanislao. Instituto de Investigaciones Médicas Aplicadas. Laboratorio de Terapia Génica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina  
dc.description.fil
Fil: Atorrasagasti, María Catalina. Instituto de Investigaciones Médicas Aplicadas. Laboratorio de Terapia Génica; Argentina. Universidad Austral. Facultad de Ciencias Biomédicas. Instituto de Investigaciones en Medicina Traslacional. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones en Medicina Traslacional; Argentina  
dc.description.fil
Fil: Malvicini, Mariana. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Instituto de Investigaciones Médicas Aplicadas. Laboratorio de Terapia Génica; Argentina  
dc.description.fil
Fil: Fiore, Esteban Juan. Instituto de Investigaciones Médicas Aplicadas. Laboratorio de Terapia Génica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina  
dc.description.fil
Fil: Rodriguez, Marcelo. Instituto de Investigaciones Médicas Aplicadas. Laboratorio de Terapia Génica; Argentina  
dc.description.fil
Fil: García, Mariana Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Instituto de Investigaciones Médicas Aplicadas. Laboratorio de Terapia Génica; Argentina  
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Fil: Finocchieto, Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina  
dc.description.fil
Fil: Poderoso, Juan José. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina  
dc.description.fil
Fil: Corrales, Fernando. Cima; España  
dc.description.fil
Fil: Mazzolini Rizzo, Guillermo Daniel. Instituto de Investigaciones Médicas Aplicadas. Laboratorio de Terapia Génica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina  
dc.journal.title
Oncotarget  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=9456&path%5B%5D=29365  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.18632/oncotarget.9456