Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association

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Background: Chronic injury deregulates cellular homeostasis and induces a number of alterations leading to disruption of cellular processes such as cell cycle checkpoints and apoptosis, driving to carcinogenesis. The stress protein heme oxygenase-1 (HO-1) catalyzes heme degradation producing biliver...

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Autores principales:	Castronuovo, C.C., Sacca, P.A., Meiss, R., Caballero, F.A., Batlle, A., Vazquez, E.S.
Formato:	Artículo publishedVersion
Publicado:	2006
Materias:	4 dimethylaminoazobenzene carcinogen cell cycle protein cyclin dependent kinase 2 cyclin dependent kinase inhibitor 1 cyclin E heme oxygenase 1 protein bcl 2 animal cell animal experiment animal model animal tissue article cell type cellular distribution controlled study dietary intake enzyme analysis hepatitis homeostasis immunohistochemistry in vivo study liver cell carcinoma liver necrosis liver regeneration macrophage male mouse mouse strain nonhuman oxidative stress protein expression protein induction Western blotting Animals Carcinogens Carcinoma, Hepatocellular Cell Cycle Cell Cycle Proteins Drug Administration Schedule Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Heme Oxygenase-1 Homeostasis Liver Neoplasms Male Mice Mice, Inbred Strains p-Dimethylaminoazobenzene
Acceso en línea:	http://hdl.handle.net/20.500.12110/paper_14712407_v6_n_p_Castronuovo http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_14712407_v6_n_p_Castronuovo_oai
Aporte de:	Repositorio Digital de la Universidad de Buenos Aires (UBA) de Universidad de Buenos Aires

id	I28-R145-paper_14712407_v6_n_p_Castronuovo_oai
record_format	dspace
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-145
collection	Repositorio Digital de la Universidad de Buenos Aires (UBA)
topic	4 dimethylaminoazobenzene carcinogen cell cycle protein cyclin dependent kinase 2 cyclin dependent kinase inhibitor 1 cyclin E heme oxygenase 1 protein bcl 2 animal cell animal experiment animal model animal tissue article cell type cellular distribution controlled study dietary intake enzyme analysis hepatitis homeostasis immunohistochemistry in vivo study liver cell carcinoma liver necrosis liver regeneration macrophage male mouse mouse strain nonhuman oxidative stress protein expression protein induction Western blotting Animals Carcinogens Carcinoma, Hepatocellular Cell Cycle Cell Cycle Proteins Drug Administration Schedule Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Heme Oxygenase-1 Homeostasis Liver Neoplasms Male Mice Mice, Inbred Strains p-Dimethylaminoazobenzene
spellingShingle	4 dimethylaminoazobenzene carcinogen cell cycle protein cyclin dependent kinase 2 cyclin dependent kinase inhibitor 1 cyclin E heme oxygenase 1 protein bcl 2 animal cell animal experiment animal model animal tissue article cell type cellular distribution controlled study dietary intake enzyme analysis hepatitis homeostasis immunohistochemistry in vivo study liver cell carcinoma liver necrosis liver regeneration macrophage male mouse mouse strain nonhuman oxidative stress protein expression protein induction Western blotting Animals Carcinogens Carcinoma, Hepatocellular Cell Cycle Cell Cycle Proteins Drug Administration Schedule Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Heme Oxygenase-1 Homeostasis Liver Neoplasms Male Mice Mice, Inbred Strains p-Dimethylaminoazobenzene Castronuovo, C.C. Sacca, P.A. Meiss, R. Caballero, F.A. Batlle, A. Vazquez, E.S. Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association
topic_facet	4 dimethylaminoazobenzene carcinogen cell cycle protein cyclin dependent kinase 2 cyclin dependent kinase inhibitor 1 cyclin E heme oxygenase 1 protein bcl 2 animal cell animal experiment animal model animal tissue article cell type cellular distribution controlled study dietary intake enzyme analysis hepatitis homeostasis immunohistochemistry in vivo study liver cell carcinoma liver necrosis liver regeneration macrophage male mouse mouse strain nonhuman oxidative stress protein expression protein induction Western blotting Animals Carcinogens Carcinoma, Hepatocellular Cell Cycle Cell Cycle Proteins Drug Administration Schedule Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Heme Oxygenase-1 Homeostasis Liver Neoplasms Male Mice Mice, Inbred Strains p-Dimethylaminoazobenzene
description	Background: Chronic injury deregulates cellular homeostasis and induces a number of alterations leading to disruption of cellular processes such as cell cycle checkpoints and apoptosis, driving to carcinogenesis. The stress protein heme oxygenase-1 (HO-1) catalyzes heme degradation producing biliverdin, iron and CO. Induction of HO-1 has been suggested to be essential for a controlled cell growth. The aim of this work was to analyze the in vivo homeostatic response (HR) triggered by the withdrawal of a potent carcinogen, p-dimethylaminoazobenzene (DAB), after preneoplastic lesions were observed. We analyzed HO-1 cellular localization and the expression of HO-1, Bcl-2 and cell cycle related proteins under these conditions comparing them to hepatocellular carcinoma (HC). Methods: The intoxication protocol was designed based on previous studies demonstrating that preneoplastic lesions were evident after 89 days of chemical carcinogen administration. Male CF1 mice (n = 18) were used. HR group received DAB (0.5 % w/w) in the diet for 78 days followed by 11 days of carcinogen deprivation. The HC group received the carcinogen and control animals the standard diet during 89 days. The expression of cell cycle related proteins, of Bcl-2 and of HO-1 were analyzed by western blot. The cellular localization and expression of HO-1 were detected by immnunohistochemistry. Results: Increased expression of cyclin E/CDK2 was observed in HR, thus implicating cyclin E/CDK2 in the liver regenerative process. p21cip1/waf1 and Bcl-2 induction in HC was restituted to basal levels in HR. A similar response profile was found for HO-1 expression levels, showing a lower oxidative status in the carcinogen-deprived liver. The immunohistochemical studies revealed the presence of macrophages surrounding foci of necrosis and nodular lesions in HR indicative of an inflammatory response. Furthermore, regenerative cells displayed changes in type, size and intensity of HO-1 immunostaining. Conclusion: These results demonstrate that the regenera tive capacity of the liver is still observed in the pre-neoplastic tissue after carcinogen withdrawal suggesting that reversible mechanism/s to compensate necrosis and to restitute homeostasis are involved. © 2006 Castronuovo et al; licensee BioMed Central Ltd.
format	Artículo Artículo publishedVersion
author	Castronuovo, C.C. Sacca, P.A. Meiss, R. Caballero, F.A. Batlle, A. Vazquez, E.S.
author_facet	Castronuovo, C.C. Sacca, P.A. Meiss, R. Caballero, F.A. Batlle, A. Vazquez, E.S.
author_sort	Castronuovo, C.C.
title	Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association
title_short	Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association
title_full	Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association
title_fullStr	Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association
title_full_unstemmed	Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association
title_sort	homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association
publishDate	2006
url	http://hdl.handle.net/20.500.12110/paper_14712407_v6_n_p_Castronuovo http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_14712407_v6_n_p_Castronuovo_oai
work_keys_str_mv	AT castronuovocc homeostaticresponseundercarcinogenwithdrawalhemeoxygenase1expressionandcellcycleassociation AT saccapa homeostaticresponseundercarcinogenwithdrawalhemeoxygenase1expressionandcellcycleassociation AT meissr homeostaticresponseundercarcinogenwithdrawalhemeoxygenase1expressionandcellcycleassociation AT caballerofa homeostaticresponseundercarcinogenwithdrawalhemeoxygenase1expressionandcellcycleassociation AT batllea homeostaticresponseundercarcinogenwithdrawalhemeoxygenase1expressionandcellcycleassociation AT vazquezes homeostaticresponseundercarcinogenwithdrawalhemeoxygenase1expressionandcellcycleassociation
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spelling	I28-R145-paper_14712407_v6_n_p_Castronuovo_oai2020-10-19 Castronuovo, C.C. Sacca, P.A. Meiss, R. Caballero, F.A. Batlle, A. Vazquez, E.S. 2006 Background: Chronic injury deregulates cellular homeostasis and induces a number of alterations leading to disruption of cellular processes such as cell cycle checkpoints and apoptosis, driving to carcinogenesis. The stress protein heme oxygenase-1 (HO-1) catalyzes heme degradation producing biliverdin, iron and CO. Induction of HO-1 has been suggested to be essential for a controlled cell growth. The aim of this work was to analyze the in vivo homeostatic response (HR) triggered by the withdrawal of a potent carcinogen, p-dimethylaminoazobenzene (DAB), after preneoplastic lesions were observed. We analyzed HO-1 cellular localization and the expression of HO-1, Bcl-2 and cell cycle related proteins under these conditions comparing them to hepatocellular carcinoma (HC). Methods: The intoxication protocol was designed based on previous studies demonstrating that preneoplastic lesions were evident after 89 days of chemical carcinogen administration. Male CF1 mice (n = 18) were used. HR group received DAB (0.5 % w/w) in the diet for 78 days followed by 11 days of carcinogen deprivation. The HC group received the carcinogen and control animals the standard diet during 89 days. The expression of cell cycle related proteins, of Bcl-2 and of HO-1 were analyzed by western blot. The cellular localization and expression of HO-1 were detected by immnunohistochemistry. Results: Increased expression of cyclin E/CDK2 was observed in HR, thus implicating cyclin E/CDK2 in the liver regenerative process. p21cip1/waf1 and Bcl-2 induction in HC was restituted to basal levels in HR. A similar response profile was found for HO-1 expression levels, showing a lower oxidative status in the carcinogen-deprived liver. The immunohistochemical studies revealed the presence of macrophages surrounding foci of necrosis and nodular lesions in HR indicative of an inflammatory response. Furthermore, regenerative cells displayed changes in type, size and intensity of HO-1 immunostaining. Conclusion: These results demonstrate that the regenera tive capacity of the liver is still observed in the pre-neoplastic tissue after carcinogen withdrawal suggesting that reversible mechanism/s to compensate necrosis and to restitute homeostasis are involved. © 2006 Castronuovo et al; licensee BioMed Central Ltd. Fil:Castronuovo, C.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Sacca, P.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Batlle, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Vazquez, E.S. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. application/pdf http://hdl.handle.net/20.500.12110/paper_14712407_v6_n_p_Castronuovo info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar BMC Cancer 2006;6 4 dimethylaminoazobenzene carcinogen cell cycle protein cyclin dependent kinase 2 cyclin dependent kinase inhibitor 1 cyclin E heme oxygenase 1 protein bcl 2 animal cell animal experiment animal model animal tissue article cell type cellular distribution controlled study dietary intake enzyme analysis hepatitis homeostasis immunohistochemistry in vivo study liver cell carcinoma liver necrosis liver regeneration macrophage male mouse mouse strain nonhuman oxidative stress protein expression protein induction Western blotting Animals Carcinogens Carcinoma, Hepatocellular Cell Cycle Cell Cycle Proteins Drug Administration Schedule Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Heme Oxygenase-1 Homeostasis Liver Neoplasms Male Mice Mice, Inbred Strains p-Dimethylaminoazobenzene Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association info:eu-repo/semantics/article info:ar-repo/semantics/artículo info:eu-repo/semantics/publishedVersion http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=artiaex&d=paper_14712407_v6_n_p_Castronuovo_oai

Homeostatic response under carcinogen withdrawal, heme oxygenase 1 expression and cell cycle association

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