Superoxide overproduction and kidney fibrosis: a new animal model

Detalhes bibliográficos
Autor(a) principal: Guimarães-Souza,Nadia Karina
Data de Publicação: 2015
Outros Autores: Yamaleyeva,Liliya Marsovna, Lu,Baisong, Ramos,Ana Claudia Mallet de Souza, Bishop,Colin Edward, Andersson,Karl Erik
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Einstein (São Paulo)
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082015000100014
Resumo: Objective To establish whether the mutation in the Immp2L gene induces renal fibrosis and whether aging exacerbates renal morphology in mice. Methods Female mutant mice with mutation in the inner mitochondrial membrane peptidase 2-like protein at 3 and 18 months of age were used. Renal fibrosis was analyzed using classic fibrosis score, Masson’s trichrome staining, and analysis of profibrotic markers using real time polymerase chain reaction (superoxide dismutase 1, metalloproteinase-9, erythropoietin, transforming growth factor beta), and immunostaining (fibroblasts and Type IV collagen). Oxidative stress markers were determined by immunohistochemistry. The number of renal apoptotic cells was determined. Renal function was estimated by serum creatinine. Results Young mutant mice had significantly more glomerulosclerosis than age-matched mice (p=0.034). Mutant mice had more tubular casts (p=0.025), collagen deposition (p=0.019), and collagen type IV expression (p<0.001). Superoxide dismutase 1 expression was significantly higher in young mutants (p=0.038). Old mutants exhibited significantly higher expression of the fibroblast marker and macrophage marker (p=0.007 and p=0.012, respectively). The real time polymerase chain reaction of metalloproteinase-9 and erythropoietin were enhanced 2.5- and 6-fold, respectively, in old mutants. Serum creatinine was significantly higher in old mutants (p<0.001). Conclusion This mutation altered renal architecture by increasing the deposition of extracellular matrix, oxidative stress, and inflammation, suggesting a protective role of Immp2L against renal fibrosis.
id IIEPAE-1_55855598854e178c3bf56725cb30baf3
oai_identifier_str oai:scielo:S1679-45082015000100014
network_acronym_str IIEPAE-1
network_name_str Einstein (São Paulo)
repository_id_str
spelling Superoxide overproduction and kidney fibrosis: a new animal modelRenal insufficiency, chronicInflammationMice, transgenicModels, animalOxidative stress Objective To establish whether the mutation in the Immp2L gene induces renal fibrosis and whether aging exacerbates renal morphology in mice. Methods Female mutant mice with mutation in the inner mitochondrial membrane peptidase 2-like protein at 3 and 18 months of age were used. Renal fibrosis was analyzed using classic fibrosis score, Masson’s trichrome staining, and analysis of profibrotic markers using real time polymerase chain reaction (superoxide dismutase 1, metalloproteinase-9, erythropoietin, transforming growth factor beta), and immunostaining (fibroblasts and Type IV collagen). Oxidative stress markers were determined by immunohistochemistry. The number of renal apoptotic cells was determined. Renal function was estimated by serum creatinine. Results Young mutant mice had significantly more glomerulosclerosis than age-matched mice (p=0.034). Mutant mice had more tubular casts (p=0.025), collagen deposition (p=0.019), and collagen type IV expression (p<0.001). Superoxide dismutase 1 expression was significantly higher in young mutants (p=0.038). Old mutants exhibited significantly higher expression of the fibroblast marker and macrophage marker (p=0.007 and p=0.012, respectively). The real time polymerase chain reaction of metalloproteinase-9 and erythropoietin were enhanced 2.5- and 6-fold, respectively, in old mutants. Serum creatinine was significantly higher in old mutants (p<0.001). Conclusion This mutation altered renal architecture by increasing the deposition of extracellular matrix, oxidative stress, and inflammation, suggesting a protective role of Immp2L against renal fibrosis. Instituto Israelita de Ensino e Pesquisa Albert Einstein2015-03-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082015000100014einstein (São Paulo) v.13 n.1 2015reponame:Einstein (São Paulo)instname:Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)instacron:IIEPAE10.1590/S1679-45082015AO3179info:eu-repo/semantics/openAccessGuimarães-Souza,Nadia KarinaYamaleyeva,Liliya MarsovnaLu,BaisongRamos,Ana Claudia Mallet de SouzaBishop,Colin EdwardAndersson,Karl Erikeng2015-08-03T00:00:00Zoai:scielo:S1679-45082015000100014Revistahttps://journal.einstein.br/pt-br/ONGhttps://old.scielo.br/oai/scielo-oai.php||revista@einstein.br2317-63851679-4508opendoar:2015-08-03T00:00Einstein (São Paulo) - Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)false
dc.title.none.fl_str_mv Superoxide overproduction and kidney fibrosis: a new animal model
title Superoxide overproduction and kidney fibrosis: a new animal model
spellingShingle Superoxide overproduction and kidney fibrosis: a new animal model
Guimarães-Souza,Nadia Karina
Renal insufficiency, chronic
Inflammation
Mice, transgenic
Models, animal
Oxidative stress
title_short Superoxide overproduction and kidney fibrosis: a new animal model
title_full Superoxide overproduction and kidney fibrosis: a new animal model
title_fullStr Superoxide overproduction and kidney fibrosis: a new animal model
title_full_unstemmed Superoxide overproduction and kidney fibrosis: a new animal model
title_sort Superoxide overproduction and kidney fibrosis: a new animal model
author Guimarães-Souza,Nadia Karina
author_facet Guimarães-Souza,Nadia Karina
Yamaleyeva,Liliya Marsovna
Lu,Baisong
Ramos,Ana Claudia Mallet de Souza
Bishop,Colin Edward
Andersson,Karl Erik
author_role author
author2 Yamaleyeva,Liliya Marsovna
Lu,Baisong
Ramos,Ana Claudia Mallet de Souza
Bishop,Colin Edward
Andersson,Karl Erik
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Guimarães-Souza,Nadia Karina
Yamaleyeva,Liliya Marsovna
Lu,Baisong
Ramos,Ana Claudia Mallet de Souza
Bishop,Colin Edward
Andersson,Karl Erik
dc.subject.por.fl_str_mv Renal insufficiency, chronic
Inflammation
Mice, transgenic
Models, animal
Oxidative stress
topic Renal insufficiency, chronic
Inflammation
Mice, transgenic
Models, animal
Oxidative stress
description Objective To establish whether the mutation in the Immp2L gene induces renal fibrosis and whether aging exacerbates renal morphology in mice. Methods Female mutant mice with mutation in the inner mitochondrial membrane peptidase 2-like protein at 3 and 18 months of age were used. Renal fibrosis was analyzed using classic fibrosis score, Masson’s trichrome staining, and analysis of profibrotic markers using real time polymerase chain reaction (superoxide dismutase 1, metalloproteinase-9, erythropoietin, transforming growth factor beta), and immunostaining (fibroblasts and Type IV collagen). Oxidative stress markers were determined by immunohistochemistry. The number of renal apoptotic cells was determined. Renal function was estimated by serum creatinine. Results Young mutant mice had significantly more glomerulosclerosis than age-matched mice (p=0.034). Mutant mice had more tubular casts (p=0.025), collagen deposition (p=0.019), and collagen type IV expression (p<0.001). Superoxide dismutase 1 expression was significantly higher in young mutants (p=0.038). Old mutants exhibited significantly higher expression of the fibroblast marker and macrophage marker (p=0.007 and p=0.012, respectively). The real time polymerase chain reaction of metalloproteinase-9 and erythropoietin were enhanced 2.5- and 6-fold, respectively, in old mutants. Serum creatinine was significantly higher in old mutants (p<0.001). Conclusion This mutation altered renal architecture by increasing the deposition of extracellular matrix, oxidative stress, and inflammation, suggesting a protective role of Immp2L against renal fibrosis.
publishDate 2015
dc.date.none.fl_str_mv 2015-03-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082015000100014
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1679-45082015000100014
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/S1679-45082015AO3179
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv text/html
dc.publisher.none.fl_str_mv Instituto Israelita de Ensino e Pesquisa Albert Einstein
publisher.none.fl_str_mv Instituto Israelita de Ensino e Pesquisa Albert Einstein
dc.source.none.fl_str_mv einstein (São Paulo) v.13 n.1 2015
reponame:Einstein (São Paulo)
instname:Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)
instacron:IIEPAE
instname_str Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)
instacron_str IIEPAE
institution IIEPAE
reponame_str Einstein (São Paulo)
collection Einstein (São Paulo)
repository.name.fl_str_mv Einstein (São Paulo) - Instituto Israelita de Ensino e Pesquisa Albert Einstein (IIEPAE)
repository.mail.fl_str_mv ||revista@einstein.br
_version_ 1752129907593314304