Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF
Autor(a) principal: | |
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Data de Publicação: | 2014 |
Outros Autores: | , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://onlinelibrary.wiley.com/doi/10.1111/iep.12107/full http://hdl.handle.net/11449/122892 |
Resumo: | Recent studies have shown a positive association of cancer and obesity, but the morphological and molecular mechanisms involved in this relationship are still unknown. This study analysed the impact of long-term obesity on rat prostate, focusing on stromal changes. Male adult Wistar rats were treated with high-fat diet to induce obesity, while the control group received a balanced diet. After 30 weeks of feeding, the ventral prostate was analysed by immunohistochemistry for cell proliferation, smooth muscle α-actin, vimentin, chondroitin sulphate and metalloproteinases (MMP-2 and 9). The content of androgen receptor (AR), oestrogen receptors (ERs) and vascular endothelial growth factor (VEGF) was measured by Western blotting, and activity of catalase and Glutathione-S-Transferase (GST) were quantified by enzymatic assay. Long-term obesity decreased testosterone plasma levels by 70% and resulted in stromal prostate hyperplasia, as evidenced by increased collagen fibres. Such stromal hyperplasia was associated with increased number of blood vessels and raised VEGF content, and increased expression of chondroitin sulphate, vimentin, α-actin and MMP-9. In spite of the high cell density in prostate, the proliferative activity was lower in the prostates of obese rats, indicating that hyperplasia was established during the early phases in this obesity model. AR levels increased significantly, whereas the ERα decreased in this group. Moreover, the levels of catalase and GST were changed considerably. These findings indicate that long-term obesity, besides disturbing the antioxidant control, causes intense stromal remodelling and release of factors that create an environment that can promote proliferative disorders in the gland, culminating with diffuse hyperplasia. |
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Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGFandrogen receptorhyperplasiaMMP-9obesityprostatestromal remodellingRecent studies have shown a positive association of cancer and obesity, but the morphological and molecular mechanisms involved in this relationship are still unknown. This study analysed the impact of long-term obesity on rat prostate, focusing on stromal changes. Male adult Wistar rats were treated with high-fat diet to induce obesity, while the control group received a balanced diet. After 30 weeks of feeding, the ventral prostate was analysed by immunohistochemistry for cell proliferation, smooth muscle α-actin, vimentin, chondroitin sulphate and metalloproteinases (MMP-2 and 9). The content of androgen receptor (AR), oestrogen receptors (ERs) and vascular endothelial growth factor (VEGF) was measured by Western blotting, and activity of catalase and Glutathione-S-Transferase (GST) were quantified by enzymatic assay. Long-term obesity decreased testosterone plasma levels by 70% and resulted in stromal prostate hyperplasia, as evidenced by increased collagen fibres. Such stromal hyperplasia was associated with increased number of blood vessels and raised VEGF content, and increased expression of chondroitin sulphate, vimentin, α-actin and MMP-9. In spite of the high cell density in prostate, the proliferative activity was lower in the prostates of obese rats, indicating that hyperplasia was established during the early phases in this obesity model. AR levels increased significantly, whereas the ERα decreased in this group. Moreover, the levels of catalase and GST were changed considerably. These findings indicate that long-term obesity, besides disturbing the antioxidant control, causes intense stromal remodelling and release of factors that create an environment that can promote proliferative disorders in the gland, culminating with diffuse hyperplasia.Universidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Biologia, Instituto de Biociências Letras e Ciências Exatas de São José do Rio Preto, Sao Jose do Rio Preto, Rua Cristóvão Colombo, 2265, Jardim Nazaterh, CEP 15054-000, SP, BrasilUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Biologia, Instituto de Biociências Letras e Ciências Exatas de São José do Rio Preto, Sao Jose do Rio Preto, Rua Cristóvão Colombo, 2265, Jardim Nazaterh, CEP 15054-000, SP, BrasilUniversidade Estadual Paulista (Unesp)Silva, Silas AmâncioGobbo, Marina Guimarães [UNESP]Pinto-Fochi, Maria Etelvina [UNESP]Rafacho, AlexTaboga, Sebastião Roberto [UNESP]Almeida, Eduardo Alves [UNESP]Goes, Rejane Maira [UNESP]Ribeiro, Daniele Lisboa2015-04-27T11:56:07Z2015-04-27T11:56:07Z2014info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://onlinelibrary.wiley.com/doi/10.1111/iep.12107/fullInternational Journal of Experimental Pathology, v. 96, p. n/a-n/a, 2014.0959-9673http://hdl.handle.net/11449/12289210.1111/iep.12107144525946852618809471933473121570000-0002-0970-42880000-0002-3622-460XCurrículo Lattesreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengInternational Journal of Experimental Pathology1.9380,712info:eu-repo/semantics/openAccess2021-10-23T21:50:45Zoai:repositorio.unesp.br:11449/122892Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462021-10-23T21:50:45Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF |
title |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF |
spellingShingle |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF Silva, Silas Amâncio androgen receptor hyperplasia MMP-9 obesity prostate stromal remodelling |
title_short |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF |
title_full |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF |
title_fullStr |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF |
title_full_unstemmed |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF |
title_sort |
Prostate hyperplasia caused by long-term obesity is characterized by high deposition of extracellular matrix and increased content of MMP-9 and VEGF |
author |
Silva, Silas Amâncio |
author_facet |
Silva, Silas Amâncio Gobbo, Marina Guimarães [UNESP] Pinto-Fochi, Maria Etelvina [UNESP] Rafacho, Alex Taboga, Sebastião Roberto [UNESP] Almeida, Eduardo Alves [UNESP] Goes, Rejane Maira [UNESP] Ribeiro, Daniele Lisboa |
author_role |
author |
author2 |
Gobbo, Marina Guimarães [UNESP] Pinto-Fochi, Maria Etelvina [UNESP] Rafacho, Alex Taboga, Sebastião Roberto [UNESP] Almeida, Eduardo Alves [UNESP] Goes, Rejane Maira [UNESP] Ribeiro, Daniele Lisboa |
author2_role |
author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade Estadual Paulista (Unesp) |
dc.contributor.author.fl_str_mv |
Silva, Silas Amâncio Gobbo, Marina Guimarães [UNESP] Pinto-Fochi, Maria Etelvina [UNESP] Rafacho, Alex Taboga, Sebastião Roberto [UNESP] Almeida, Eduardo Alves [UNESP] Goes, Rejane Maira [UNESP] Ribeiro, Daniele Lisboa |
dc.subject.por.fl_str_mv |
androgen receptor hyperplasia MMP-9 obesity prostate stromal remodelling |
topic |
androgen receptor hyperplasia MMP-9 obesity prostate stromal remodelling |
description |
Recent studies have shown a positive association of cancer and obesity, but the morphological and molecular mechanisms involved in this relationship are still unknown. This study analysed the impact of long-term obesity on rat prostate, focusing on stromal changes. Male adult Wistar rats were treated with high-fat diet to induce obesity, while the control group received a balanced diet. After 30 weeks of feeding, the ventral prostate was analysed by immunohistochemistry for cell proliferation, smooth muscle α-actin, vimentin, chondroitin sulphate and metalloproteinases (MMP-2 and 9). The content of androgen receptor (AR), oestrogen receptors (ERs) and vascular endothelial growth factor (VEGF) was measured by Western blotting, and activity of catalase and Glutathione-S-Transferase (GST) were quantified by enzymatic assay. Long-term obesity decreased testosterone plasma levels by 70% and resulted in stromal prostate hyperplasia, as evidenced by increased collagen fibres. Such stromal hyperplasia was associated with increased number of blood vessels and raised VEGF content, and increased expression of chondroitin sulphate, vimentin, α-actin and MMP-9. In spite of the high cell density in prostate, the proliferative activity was lower in the prostates of obese rats, indicating that hyperplasia was established during the early phases in this obesity model. AR levels increased significantly, whereas the ERα decreased in this group. Moreover, the levels of catalase and GST were changed considerably. These findings indicate that long-term obesity, besides disturbing the antioxidant control, causes intense stromal remodelling and release of factors that create an environment that can promote proliferative disorders in the gland, culminating with diffuse hyperplasia. |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014 2015-04-27T11:56:07Z 2015-04-27T11:56:07Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://onlinelibrary.wiley.com/doi/10.1111/iep.12107/full International Journal of Experimental Pathology, v. 96, p. n/a-n/a, 2014. 0959-9673 http://hdl.handle.net/11449/122892 10.1111/iep.12107 1445259468526188 0947193347312157 0000-0002-0970-4288 0000-0002-3622-460X |
url |
http://onlinelibrary.wiley.com/doi/10.1111/iep.12107/full http://hdl.handle.net/11449/122892 |
identifier_str_mv |
International Journal of Experimental Pathology, v. 96, p. n/a-n/a, 2014. 0959-9673 10.1111/iep.12107 1445259468526188 0947193347312157 0000-0002-0970-4288 0000-0002-3622-460X |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
International Journal of Experimental Pathology 1.938 0,712 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.source.none.fl_str_mv |
Currículo Lattes reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1803045903453388800 |