Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS

Detalhes bibliográficos
Autor(a) principal: Gloria,Maria Aparecida da
Data de Publicação: 2020
Outros Autores: Mouro,Margaret Gori, Geraldini,Simone, Higa,Elisa Mieko Suemitsu, Carvalho,Aluizio Barbosa
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Jornal Brasileiro de Nefrologia
Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002020000300300
Resumo: ABSTRACT Introduction: Vascular calcification is a common complication of chronic kidney disease. Osteoblast differentiation factor (Cbfa1) is present in histologic sections of arteries from patients with end-stage renal disease. Vascular smooth muscle cells (VSMC) can dedifferentiate to osteoblast-like cells, possibly by up-regulation of Cbfa1. There is evidence that the production of nitric oxide (NO) may have an important role in the regulation of osteoblast metabolism. The aim of this study is to evaluate whether increased NO/iNOS expression causes an increase in cbfa1 expression in VSMC. Methods: VSMC were obtained from renal artery of Wistar male rats, treated for 72 hours with lipopolysaccharide (LPS), ß-glycerophosphate (BGF), a donor of phosphate and aminoguanidine (AG), an inhibitor of iNOS, in the following groups: CTL (control), LPS, BGF, LPS + BGF, and LPS + AG. NO synthesis was determined by chemiluminescence. Cbfa1 and iNOS mRNA expressions were analyzed by RT-PCR, Cbfa1 protein expression by immunohistochemistry and cellular viability by acridine orange. Results: Cbfa1 and iNOS mRNA expressions were higher in LPS and LPS+ BGF vs CTL (p < 0.05), and they were lower in LPS+AG vs LPS (p < 0.05). The Cbfa1 in the groups LPS and LPS+BGF also resulted in a higher value compared to CTL (p < 0.05), and in LPS+AG it was lower compared to LPS (p < 0.05). NO was higher in LPS and LPS+BGF compared to CTL group (p < 0.05) and lower in LPS + AG compared to LPS group (p < 0.05). Cellular viability showed no statistical difference among groups. Conclusion: This study showed that increased NO/iNOS expression causes an increase in cbfa1 expression in VSMC.
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spelling Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOSCore Binding FactorsKidney diseasesMyocytes, Smooth MuscleNitric Oxide SynthaseABSTRACT Introduction: Vascular calcification is a common complication of chronic kidney disease. Osteoblast differentiation factor (Cbfa1) is present in histologic sections of arteries from patients with end-stage renal disease. Vascular smooth muscle cells (VSMC) can dedifferentiate to osteoblast-like cells, possibly by up-regulation of Cbfa1. There is evidence that the production of nitric oxide (NO) may have an important role in the regulation of osteoblast metabolism. The aim of this study is to evaluate whether increased NO/iNOS expression causes an increase in cbfa1 expression in VSMC. Methods: VSMC were obtained from renal artery of Wistar male rats, treated for 72 hours with lipopolysaccharide (LPS), ß-glycerophosphate (BGF), a donor of phosphate and aminoguanidine (AG), an inhibitor of iNOS, in the following groups: CTL (control), LPS, BGF, LPS + BGF, and LPS + AG. NO synthesis was determined by chemiluminescence. Cbfa1 and iNOS mRNA expressions were analyzed by RT-PCR, Cbfa1 protein expression by immunohistochemistry and cellular viability by acridine orange. Results: Cbfa1 and iNOS mRNA expressions were higher in LPS and LPS+ BGF vs CTL (p < 0.05), and they were lower in LPS+AG vs LPS (p < 0.05). The Cbfa1 in the groups LPS and LPS+BGF also resulted in a higher value compared to CTL (p < 0.05), and in LPS+AG it was lower compared to LPS (p < 0.05). NO was higher in LPS and LPS+BGF compared to CTL group (p < 0.05) and lower in LPS + AG compared to LPS group (p < 0.05). Cellular viability showed no statistical difference among groups. Conclusion: This study showed that increased NO/iNOS expression causes an increase in cbfa1 expression in VSMC.Sociedade Brasileira de Nefrologia2020-09-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002020000300300Brazilian Journal of Nephrology v.42 n.3 2020reponame:Jornal Brasileiro de Nefrologiainstname:Sociedade Brasileira de Nefrologia (SBN)instacron:SBN10.1590/2175-8239-jbn-2019-0166info:eu-repo/semantics/openAccessGloria,Maria Aparecida daMouro,Margaret GoriGeraldini,SimoneHiga,Elisa Mieko SuemitsuCarvalho,Aluizio Barbosaeng2020-11-20T00:00:00Zoai:scielo:S0101-28002020000300300Revistahttp://www.bjn.org.br/ONGhttps://old.scielo.br/oai/scielo-oai.php||jbn@sbn.org.br2175-82390101-2800opendoar:2020-11-20T00:00Jornal Brasileiro de Nefrologia - Sociedade Brasileira de Nefrologia (SBN)false
dc.title.none.fl_str_mv Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
title Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
spellingShingle Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
Gloria,Maria Aparecida da
Core Binding Factors
Kidney diseases
Myocytes, Smooth Muscle
Nitric Oxide Synthase
title_short Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
title_full Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
title_fullStr Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
title_full_unstemmed Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
title_sort Cbfa1 expression in vascular smooth muscle cells may be elevated by increased nitric oxide/iNOS
author Gloria,Maria Aparecida da
author_facet Gloria,Maria Aparecida da
Mouro,Margaret Gori
Geraldini,Simone
Higa,Elisa Mieko Suemitsu
Carvalho,Aluizio Barbosa
author_role author
author2 Mouro,Margaret Gori
Geraldini,Simone
Higa,Elisa Mieko Suemitsu
Carvalho,Aluizio Barbosa
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Gloria,Maria Aparecida da
Mouro,Margaret Gori
Geraldini,Simone
Higa,Elisa Mieko Suemitsu
Carvalho,Aluizio Barbosa
dc.subject.por.fl_str_mv Core Binding Factors
Kidney diseases
Myocytes, Smooth Muscle
Nitric Oxide Synthase
topic Core Binding Factors
Kidney diseases
Myocytes, Smooth Muscle
Nitric Oxide Synthase
description ABSTRACT Introduction: Vascular calcification is a common complication of chronic kidney disease. Osteoblast differentiation factor (Cbfa1) is present in histologic sections of arteries from patients with end-stage renal disease. Vascular smooth muscle cells (VSMC) can dedifferentiate to osteoblast-like cells, possibly by up-regulation of Cbfa1. There is evidence that the production of nitric oxide (NO) may have an important role in the regulation of osteoblast metabolism. The aim of this study is to evaluate whether increased NO/iNOS expression causes an increase in cbfa1 expression in VSMC. Methods: VSMC were obtained from renal artery of Wistar male rats, treated for 72 hours with lipopolysaccharide (LPS), ß-glycerophosphate (BGF), a donor of phosphate and aminoguanidine (AG), an inhibitor of iNOS, in the following groups: CTL (control), LPS, BGF, LPS + BGF, and LPS + AG. NO synthesis was determined by chemiluminescence. Cbfa1 and iNOS mRNA expressions were analyzed by RT-PCR, Cbfa1 protein expression by immunohistochemistry and cellular viability by acridine orange. Results: Cbfa1 and iNOS mRNA expressions were higher in LPS and LPS+ BGF vs CTL (p < 0.05), and they were lower in LPS+AG vs LPS (p < 0.05). The Cbfa1 in the groups LPS and LPS+BGF also resulted in a higher value compared to CTL (p < 0.05), and in LPS+AG it was lower compared to LPS (p < 0.05). NO was higher in LPS and LPS+BGF compared to CTL group (p < 0.05) and lower in LPS + AG compared to LPS group (p < 0.05). Cellular viability showed no statistical difference among groups. Conclusion: This study showed that increased NO/iNOS expression causes an increase in cbfa1 expression in VSMC.
publishDate 2020
dc.date.none.fl_str_mv 2020-09-01
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=S0101-28002020000300300
url http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-28002020000300300
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv 10.1590/2175-8239-jbn-2019-0166
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 Sociedade Brasileira de Nefrologia
publisher.none.fl_str_mv Sociedade Brasileira de Nefrologia
dc.source.none.fl_str_mv Brazilian Journal of Nephrology v.42 n.3 2020
reponame:Jornal Brasileiro de Nefrologia
instname:Sociedade Brasileira de Nefrologia (SBN)
instacron:SBN
instname_str Sociedade Brasileira de Nefrologia (SBN)
instacron_str SBN
institution SBN
reponame_str Jornal Brasileiro de Nefrologia
collection Jornal Brasileiro de Nefrologia
repository.name.fl_str_mv Jornal Brasileiro de Nefrologia - Sociedade Brasileira de Nefrologia (SBN)
repository.mail.fl_str_mv ||jbn@sbn.org.br
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