Transforming growth factor-β in graft vessels: histology and immunohistochemistry
Autor(a) principal: | |
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Data de Publicação: | 2011 |
Outros Autores: | , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Clinics |
Texto Completo: | https://www.revistas.usp.br/clinics/article/view/19570 |
Resumo: | OBJECTIVES: The biological functions of transforming growth factor-β signaling that involves Smad proteins have not been previously investigated with respect to coronary artery bypass grafts. The aim of the present study was to observe the immunostaining of proteins that are related to this signaling pathway. METHODS: Fifteen remnants of coronary artery bypass grafts, including nine saphenous veins, three radial arteries and three mammary arteries, were collected from 12 patients who were undergoing coronary artery bypass. Hematoxylin and eosin, Masson's trichrome, and immunohistochemical staining of transforming growth factor-β1, type I receptor of transforming growth factor-β, Smad2/3, Smad4, and Smad7 were performed. RESULTS: The saphenous veins showed more severe intimal degeneration, more severe smooth muscle cell proliferation and more collagen deposition than the arterial grafts, as evidenced by hematoxylin and eosin and Masson's trichrome stainings. Immunohistochemical assays demonstrated that the majority of the transforming growth factor-β1 signaling cytokines were primarily localized in the cytoplasm in the medial layers of all three types of grafts, whereas ectopic transforming growth factor-β1, type I receptor of transforming growth factor-β, and Smad7 overexpressions in the interstices were observed particularly in the saphenous vein and radial arterial grafts. CONCLUSION: Enhanced transforming growth factor-β1 signal transduction with medial smooth muscle cell proliferation and ectopic transforming growth factor-β1, the presence of the type I receptor of transforming growth factor-β, and Smad7 overexpressions in the extracellular matrix may provide primary evidence for early or late graft failure. |
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Transforming growth factor-β in graft vessels: histology and immunohistochemistry Blood VesselsCoronary Artery BypassImmunohistochemistrySignal TransductionTransforming Growth Factor-β OBJECTIVES: The biological functions of transforming growth factor-β signaling that involves Smad proteins have not been previously investigated with respect to coronary artery bypass grafts. The aim of the present study was to observe the immunostaining of proteins that are related to this signaling pathway. METHODS: Fifteen remnants of coronary artery bypass grafts, including nine saphenous veins, three radial arteries and three mammary arteries, were collected from 12 patients who were undergoing coronary artery bypass. Hematoxylin and eosin, Masson's trichrome, and immunohistochemical staining of transforming growth factor-β1, type I receptor of transforming growth factor-β, Smad2/3, Smad4, and Smad7 were performed. RESULTS: The saphenous veins showed more severe intimal degeneration, more severe smooth muscle cell proliferation and more collagen deposition than the arterial grafts, as evidenced by hematoxylin and eosin and Masson's trichrome stainings. Immunohistochemical assays demonstrated that the majority of the transforming growth factor-β1 signaling cytokines were primarily localized in the cytoplasm in the medial layers of all three types of grafts, whereas ectopic transforming growth factor-β1, type I receptor of transforming growth factor-β, and Smad7 overexpressions in the interstices were observed particularly in the saphenous vein and radial arterial grafts. CONCLUSION: Enhanced transforming growth factor-β1 signal transduction with medial smooth muscle cell proliferation and ectopic transforming growth factor-β1, the presence of the type I receptor of transforming growth factor-β, and Smad7 overexpressions in the extracellular matrix may provide primary evidence for early or late graft failure. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2011-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/1957010.1590/S1807-59322011000500029Clinics; Vol. 66 No. 5 (2011); 895-901 Clinics; v. 66 n. 5 (2011); 895-901 Clinics; Vol. 66 Núm. 5 (2011); 895-901 1980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/19570/21633Yuan, Shi-MinWang, Yan-QingShen, YiJing, Huainfo:eu-repo/semantics/openAccess2012-05-23T16:49:18Zoai:revistas.usp.br:article/19570Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2012-05-23T16:49:18Clinics - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry |
title |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry |
spellingShingle |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry Yuan, Shi-Min Blood Vessels Coronary Artery Bypass Immunohistochemistry Signal Transduction Transforming Growth Factor-β |
title_short |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry |
title_full |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry |
title_fullStr |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry |
title_full_unstemmed |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry |
title_sort |
Transforming growth factor-β in graft vessels: histology and immunohistochemistry |
author |
Yuan, Shi-Min |
author_facet |
Yuan, Shi-Min Wang, Yan-Qing Shen, Yi Jing, Hua |
author_role |
author |
author2 |
Wang, Yan-Qing Shen, Yi Jing, Hua |
author2_role |
author author author |
dc.contributor.author.fl_str_mv |
Yuan, Shi-Min Wang, Yan-Qing Shen, Yi Jing, Hua |
dc.subject.por.fl_str_mv |
Blood Vessels Coronary Artery Bypass Immunohistochemistry Signal Transduction Transforming Growth Factor-β |
topic |
Blood Vessels Coronary Artery Bypass Immunohistochemistry Signal Transduction Transforming Growth Factor-β |
description |
OBJECTIVES: The biological functions of transforming growth factor-β signaling that involves Smad proteins have not been previously investigated with respect to coronary artery bypass grafts. The aim of the present study was to observe the immunostaining of proteins that are related to this signaling pathway. METHODS: Fifteen remnants of coronary artery bypass grafts, including nine saphenous veins, three radial arteries and three mammary arteries, were collected from 12 patients who were undergoing coronary artery bypass. Hematoxylin and eosin, Masson's trichrome, and immunohistochemical staining of transforming growth factor-β1, type I receptor of transforming growth factor-β, Smad2/3, Smad4, and Smad7 were performed. RESULTS: The saphenous veins showed more severe intimal degeneration, more severe smooth muscle cell proliferation and more collagen deposition than the arterial grafts, as evidenced by hematoxylin and eosin and Masson's trichrome stainings. Immunohistochemical assays demonstrated that the majority of the transforming growth factor-β1 signaling cytokines were primarily localized in the cytoplasm in the medial layers of all three types of grafts, whereas ectopic transforming growth factor-β1, type I receptor of transforming growth factor-β, and Smad7 overexpressions in the interstices were observed particularly in the saphenous vein and radial arterial grafts. CONCLUSION: Enhanced transforming growth factor-β1 signal transduction with medial smooth muscle cell proliferation and ectopic transforming growth factor-β1, the presence of the type I receptor of transforming growth factor-β, and Smad7 overexpressions in the extracellular matrix may provide primary evidence for early or late graft failure. |
publishDate |
2011 |
dc.date.none.fl_str_mv |
2011-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://www.revistas.usp.br/clinics/article/view/19570 10.1590/S1807-59322011000500029 |
url |
https://www.revistas.usp.br/clinics/article/view/19570 |
identifier_str_mv |
10.1590/S1807-59322011000500029 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://www.revistas.usp.br/clinics/article/view/19570/21633 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
publisher.none.fl_str_mv |
Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo |
dc.source.none.fl_str_mv |
Clinics; Vol. 66 No. 5 (2011); 895-901 Clinics; v. 66 n. 5 (2011); 895-901 Clinics; Vol. 66 Núm. 5 (2011); 895-901 1980-5322 1807-5932 reponame:Clinics instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Clinics |
collection |
Clinics |
repository.name.fl_str_mv |
Clinics - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
||clinics@hc.fm.usp.br |
_version_ |
1800222757799067648 |