Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis

Background: Nickel and nickel-containing compounds (NCC) are known human carcinogens. However, the precise molecular mechanisms of nickel-induced malignant transformation remain unknown. Proposed mechanisms suggest that nickel and NCC may participate in the dual activation/inactivation of enzymatic...

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Autores:
Jiménez-Vidal, Luisa
Espitia-Pérez, Pedro
Torres-Ávila, José
Ricardo-Caldera, Dina
Salcedo-Arteaga, Shirley
Galeano-Páez, Claudia
Pastor-Sierra, Karina
Espitia-Pérez, Lyda
Tipo de recurso:
Fecha de publicación:
2019
Institución:
Universidad Simón Bolívar
Repositorio:
Repositorio Digital USB
Idioma:
eng
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oai:bonga.unisimon.edu.co:20.500.12442/4599
Acceso en línea:
https://hdl.handle.net/20.500.12442/4599
Palabra clave:
Nickel
Nrf2
ER-stress
UPR
NiSO4
Ni3S2
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Attribution-NonCommercial-NoDerivatives 4.0 Internacional
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network_acronym_str USIMONBOL2
network_name_str Repositorio Digital USB
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dc.title.eng.fl_str_mv Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
title Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
spellingShingle Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
Nickel
Nrf2
ER-stress
UPR
NiSO4
Ni3S2
title_short Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
title_full Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
title_fullStr Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
title_full_unstemmed Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
title_sort Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysis
dc.creator.fl_str_mv Jiménez-Vidal, Luisa
Espitia-Pérez, Pedro
Torres-Ávila, José
Ricardo-Caldera, Dina
Salcedo-Arteaga, Shirley
Galeano-Páez, Claudia
Pastor-Sierra, Karina
Espitia-Pérez, Lyda
dc.contributor.author.none.fl_str_mv Jiménez-Vidal, Luisa
Espitia-Pérez, Pedro
Torres-Ávila, José
Ricardo-Caldera, Dina
Salcedo-Arteaga, Shirley
Galeano-Páez, Claudia
Pastor-Sierra, Karina
Espitia-Pérez, Lyda
dc.subject.eng.fl_str_mv Nickel
Nrf2
ER-stress
UPR
NiSO4
Ni3S2
topic Nickel
Nrf2
ER-stress
UPR
NiSO4
Ni3S2
description Background: Nickel and nickel-containing compounds (NCC) are known human carcinogens. However, the precise molecular mechanisms of nickel-induced malignant transformation remain unknown. Proposed mechanisms suggest that nickel and NCC may participate in the dual activation/inactivation of enzymatic pathways involved in cell defenses against oxidative damage, where Nuclear factor-erythroid 2 related factor 2 (Nrf2) plays a central role. Methods: For assessing the potential role of proteins involved in the Nrf2-mediated response to nickel and NCC exposure, we designed an interactome network using the STITCH search engine version 5.0 and the STRING software 10.0. The major NCC-protein interactome (NCPI) generated was analyzed using the MCODE plugin, version 1.5.1 for the detection of interaction modules or subnetworks. Main centralities of the NCPI were determined with the CentiScape 2.2 plugin of Cytoscape 3.4.0 and main biological processes associated with each cluster were assessed using the BiNGO plugin of Cytoscape 3.4.0. Results: Water-soluble NiSO4 and insoluble Ni3S2 were the most connected to proteins involved in the NCPI network. Nfr2 was detected as one of the most relevant proteins in the network, participating in several multifunctional protein complexes in clusters 1, 2, 3 and 5. Ontological analysis of cluster 3 revealed several processes related to unfolded protein response (UPR) and response to endoplasmic reticulum (ER) stress. Conclusions: Cellular response to NCC exposure was very comparable, particularly concerning oxidative stress response, inflammation, cell cycle/proliferation, and apoptosis. In this cellular response, Nfr2 was highly centralized and participated in several multifunctional protein complexes, including several related to ER-stress. These results add evidence on the possible Ni2+ induced – ER stress mainly associated with insoluble NCC. In this scenario, we also show how protein degradation mediated by ubiquitination seems to play key roles in cellular responses to Ni.
publishDate 2019
dc.date.issued.none.fl_str_mv 2019
dc.date.accessioned.none.fl_str_mv 2020-01-29T22:36:58Z
dc.date.available.none.fl_str_mv 2020-01-29T22:36:58Z
dc.type.eng.fl_str_mv article
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dc.type.driver.eng.fl_str_mv article
dc.identifier.issn.none.fl_str_mv 20506511
dc.identifier.uri.none.fl_str_mv https://hdl.handle.net/20.500.12442/4599
identifier_str_mv 20506511
url https://hdl.handle.net/20.500.12442/4599
dc.language.iso.eng.fl_str_mv eng
language eng
dc.rights.none.fl_str_mv Attribution-NonCommercial-NoDerivatives 4.0 Internacional
dc.rights.coar.fl_str_mv http://purl.org/coar/access_right/c_abf2
dc.rights.uri.none.fl_str_mv http://creativecommons.org/licenses/by-nc-nd/4.0/
rights_invalid_str_mv Attribution-NonCommercial-NoDerivatives 4.0 Internacional
http://creativecommons.org/licenses/by-nc-nd/4.0/
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dc.format.mimetype.spa.fl_str_mv pdf
dc.publisher.eng.fl_str_mv BMC
dc.source.eng.fl_str_mv BMC Pharmacology and Toxicology
Vol. 20 (Suppl 1), (2019)
institution Universidad Simón Bolívar
dc.source.uri.eng.fl_str_mv https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6921378/pdf/40360_2019_Article_360.pdf
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spelling Jiménez-Vidal, Luisad2668ef4-2165-4a9d-b437-3608fc2dc64dEspitia-Pérez, Pedro9b91d650-d997-4d18-8816-7533217bbe79Torres-Ávila, Joséc6ad5e8a-dff2-4e2d-9487-8535f5fc2a4cRicardo-Caldera, Dinab4efd4e2-de08-4718-a509-d479fb044968Salcedo-Arteaga, Shirleyb6022871-47c5-4bf8-801d-f2d13457913bGaleano-Páez, Claudia87bf0cca-be30-4818-9e64-04edc0eb5171Pastor-Sierra, Karina3e3568bc-f7f2-49b4-9945-3c728a562227Espitia-Pérez, Lyda8c646a69-2fd1-499d-9691-d31053b5bd0b2020-01-29T22:36:58Z2020-01-29T22:36:58Z201920506511https://hdl.handle.net/20.500.12442/4599Background: Nickel and nickel-containing compounds (NCC) are known human carcinogens. However, the precise molecular mechanisms of nickel-induced malignant transformation remain unknown. Proposed mechanisms suggest that nickel and NCC may participate in the dual activation/inactivation of enzymatic pathways involved in cell defenses against oxidative damage, where Nuclear factor-erythroid 2 related factor 2 (Nrf2) plays a central role. Methods: For assessing the potential role of proteins involved in the Nrf2-mediated response to nickel and NCC exposure, we designed an interactome network using the STITCH search engine version 5.0 and the STRING software 10.0. The major NCC-protein interactome (NCPI) generated was analyzed using the MCODE plugin, version 1.5.1 for the detection of interaction modules or subnetworks. Main centralities of the NCPI were determined with the CentiScape 2.2 plugin of Cytoscape 3.4.0 and main biological processes associated with each cluster were assessed using the BiNGO plugin of Cytoscape 3.4.0. Results: Water-soluble NiSO4 and insoluble Ni3S2 were the most connected to proteins involved in the NCPI network. Nfr2 was detected as one of the most relevant proteins in the network, participating in several multifunctional protein complexes in clusters 1, 2, 3 and 5. Ontological analysis of cluster 3 revealed several processes related to unfolded protein response (UPR) and response to endoplasmic reticulum (ER) stress. Conclusions: Cellular response to NCC exposure was very comparable, particularly concerning oxidative stress response, inflammation, cell cycle/proliferation, and apoptosis. In this cellular response, Nfr2 was highly centralized and participated in several multifunctional protein complexes, including several related to ER-stress. These results add evidence on the possible Ni2+ induced – ER stress mainly associated with insoluble NCC. In this scenario, we also show how protein degradation mediated by ubiquitination seems to play key roles in cellular responses to Ni.pdfengBMCAttribution-NonCommercial-NoDerivatives 4.0 Internacionalhttp://creativecommons.org/licenses/by-nc-nd/4.0/http://purl.org/coar/access_right/c_abf2BMC Pharmacology and ToxicologyVol. 20 (Suppl 1), (2019)https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6921378/pdf/40360_2019_Article_360.pdfNickelNrf2ER-stressUPRNiSO4Ni3S2Nuclear factor erythroid 2 – related factor 2 and its relationship with cellular response in nickel exposure: a systems biology analysisarticlearticlehttp://purl.org/coar/version/c_970fb48d4fbd8a85http://purl.org/coar/resource_type/c_6501IARC. IARC Monographs on the Valuation of the Carcinogenic Risks of Chemicals to Humans: Chromium, Nickel and Welding, vol. 49. Lyon: IARC; 1990. p. 447–525.Valko M, Rhodes CJ, Moncol J, Izakovic M, Mazur M. Free radicals, metals and antioxidants in oxidative stress-induced cancer. 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