HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms

Introduction and objectives: It is well-known that signaling mediated by the hepatocyte growth factor (HGF) and its receptor c-Met in the liver is involved in the control of cellular redox status and oxidative stress, particularly through its ability to induce hepatoprotective gene expression by act...

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Autores principales:	Arturo Simoni-Nieves, Denise Clavijo-Cornejo, Soraya Salas-Silva, Alejandro Escobedo-Calvario, Leticia Bucio, Verónica Souza, María Concepción Gutiérrez-Ruiz, Roxana U. Miranda-Labra, Luis E. Gomez-Quiroz
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	p22phox NADPH oxidase HGF Hepatocytes c-Met Specialties of internal medicine RC581-951
Acceso en línea:	https://doaj.org/article/56740f135119483cab9761715dea215c
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spelling	oai:doaj.org-article:56740f135119483cab9761715dea215c2021-11-18T04:46:00ZHGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms1665-268110.1016/j.aohep.2021.100339https://doaj.org/article/56740f135119483cab9761715dea215c2021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S1665268121000387https://doaj.org/toc/1665-2681Introduction and objectives: It is well-known that signaling mediated by the hepatocyte growth factor (HGF) and its receptor c-Met in the liver is involved in the control of cellular redox status and oxidative stress, particularly through its ability to induce hepatoprotective gene expression by activating survival pathways in hepatocytes. It has been reported that HGF can regulate the expression of some members of the NADPH oxidase family in liver cells, particularly the catalytic subunits and p22phox. In the present work we were focused to characterize the mechanism of regulation of p22phox by HGF and its receptor c-Met in primary mouse hepatocytes as a key determinant for cellular redox regulation. Materials and methods: Primary mouse hepatocytes were treated with HGF (50 ng/mL) at different times. cyba expression (gene encoding p22phox) or protein content were addressed by real time RT-PCR, Western blot or immunofluorescence. Protein interactions were explored by immunoprecipitation and FRET analysis. Results: Our results provided mechanistic information supporting the transcriptional repression of cyba induced by HGF in a mechanism dependent of NF-κB activity. We identified a post-translational regulation mechanism directed by p22phox degradation by proteasome 26S, and a second mechanism mediated by p22phox sequestration by c-Met in plasma membrane. Conclusion: Our data clearly show that HGF/c-Met exerts regulation of the NADPH oxidase by a wide-range of molecular mechanisms. NADPH oxidase-derived reactive oxygen species regulated by HGF/c-Met represents one of the main mechanisms of signal transduction elicited by this growth factor.Arturo Simoni-NievesDenise Clavijo-CornejoSoraya Salas-SilvaAlejandro Escobedo-CalvarioLeticia BucioVerónica SouzaMaría Concepción Gutiérrez-RuizRoxana U. Miranda-LabraLuis E. Gomez-QuirozElsevierarticlep22phoxNADPH oxidaseHGFHepatocytesc-MetSpecialties of internal medicineRC581-951ENAnnals of Hepatology, Vol 25, Iss , Pp 100339- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	p22phox NADPH oxidase HGF Hepatocytes c-Met Specialties of internal medicine RC581-951
spellingShingle	p22phox NADPH oxidase HGF Hepatocytes c-Met Specialties of internal medicine RC581-951 Arturo Simoni-Nieves Denise Clavijo-Cornejo Soraya Salas-Silva Alejandro Escobedo-Calvario Leticia Bucio Verónica Souza María Concepción Gutiérrez-Ruiz Roxana U. Miranda-Labra Luis E. Gomez-Quiroz HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms
description	Introduction and objectives: It is well-known that signaling mediated by the hepatocyte growth factor (HGF) and its receptor c-Met in the liver is involved in the control of cellular redox status and oxidative stress, particularly through its ability to induce hepatoprotective gene expression by activating survival pathways in hepatocytes. It has been reported that HGF can regulate the expression of some members of the NADPH oxidase family in liver cells, particularly the catalytic subunits and p22phox. In the present work we were focused to characterize the mechanism of regulation of p22phox by HGF and its receptor c-Met in primary mouse hepatocytes as a key determinant for cellular redox regulation. Materials and methods: Primary mouse hepatocytes were treated with HGF (50 ng/mL) at different times. cyba expression (gene encoding p22phox) or protein content were addressed by real time RT-PCR, Western blot or immunofluorescence. Protein interactions were explored by immunoprecipitation and FRET analysis. Results: Our results provided mechanistic information supporting the transcriptional repression of cyba induced by HGF in a mechanism dependent of NF-κB activity. We identified a post-translational regulation mechanism directed by p22phox degradation by proteasome 26S, and a second mechanism mediated by p22phox sequestration by c-Met in plasma membrane. Conclusion: Our data clearly show that HGF/c-Met exerts regulation of the NADPH oxidase by a wide-range of molecular mechanisms. NADPH oxidase-derived reactive oxygen species regulated by HGF/c-Met represents one of the main mechanisms of signal transduction elicited by this growth factor.
format	article
author	Arturo Simoni-Nieves Denise Clavijo-Cornejo Soraya Salas-Silva Alejandro Escobedo-Calvario Leticia Bucio Verónica Souza María Concepción Gutiérrez-Ruiz Roxana U. Miranda-Labra Luis E. Gomez-Quiroz
author_facet	Arturo Simoni-Nieves Denise Clavijo-Cornejo Soraya Salas-Silva Alejandro Escobedo-Calvario Leticia Bucio Verónica Souza María Concepción Gutiérrez-Ruiz Roxana U. Miranda-Labra Luis E. Gomez-Quiroz
author_sort	Arturo Simoni-Nieves
title	HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms
title_short	HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms
title_full	HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms
title_fullStr	HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms
title_full_unstemmed	HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms
title_sort	hgf/c-met regulates p22phox subunit of the nadph oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/56740f135119483cab9761715dea215c
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HGF/c-Met regulates p22phox subunit of the NADPH oxidase complex in primary mouse hepatocytes by transcriptional and post-translational mechanisms

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