Superoxide overproduction and kidney fibrosis: a new animal model
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Outros Autores: | , , , , |
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. |
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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 |
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1752129907593314304 |