[Cholesterol overload in hepatocytes affects nicotinamide adenine dinucleotide phosphate oxidase (NADPH) activity abrogating hepatocyte growth factor (HGF) induced cellular protection].
The increment in the prevalence of obesity incidence in Mexico is leading to the increase in many chronic maladies, including liver diseases. It is well known that lipid-induced liver sensitization is related to the kind of lipid rather than the amount of them in the organ. Cholesterol overload in the liver aggravates the toxic effects of canonical liver insults. However, the status on the repair and survival response elicited by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and the hepatocyte growth factor (HGF) is not completely understood. In the present, work we aimed to figure out the HGF/NADPH oxidase-induced cellular protection in the hepatocyte with a cholesterol overload. Our results show that a hypercholesterolemic diet induced liver damage and steatosis in mice. The hepatocytes isolated from these animals exhibited an increase in basal NADPH oxidase activity, although transcriptional levels of some of its components were decreased. No effect on the oxidase activity was observed in HGF treatments. The protective effect of HGF was abrogated as a result of cholesterol cellular overload, calculated by a survival assay. In conclusion, the cholesterol overload in hepatocytes impairs the HGF/NADPH oxidase-induced cellular protection.
Doctorado en Biología Experimental, DCBS, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.|Laboratorio de Sinovioanálisis, Instituto Nacional de Rehabilitación, México, D.F., México.
Alberto G
AG
López-Reyes
Laboratorio de Sinovioanálisis, Instituto Nacional de Rehabilitación, México, D.F., México.
Karina
K
Martínez-Flores
Laboratorio de Sinovioanálisis, Instituto Nacional de Rehabilitación, México, D.F., México.
Denise
D
Clavijo-Cornejo
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.
Natalia
N
Nuño-Lámbarri
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.
Mayrel
M
Palestino-Domínguez
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.|Red Fisiopatología de las Enfermedades Hepáticas, PROMEP-SEP, México D.F., México.
Verónica
V
Souza
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.|Red Fisiopatología de las Enfermedades Hepáticas, PROMEP-SEP, México D.F., México.
Leticia
L
Bucio
Red Fisiopatología de las Enfermedades Hepáticas, PROMEP-SEP, México D.F., México.|Departamento de Biología Molecular en Medicina, Hospital Civil de Guadalajara Fray Antonio Alcalde, Universidad de Guadalajara, Guadalajara, Jal., México.
Arturo
A
Panduro
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.|Red Fisiopatología de las Enfermedades Hepáticas, PROMEP-SEP, México D.F., México.
Roxana U
RU
Miranda
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.|Red Fisiopatología de las Enfermedades Hepáticas, PROMEP-SEP, México D.F., México.
Luis Enrique
LE
Gómez-Quiroz
Departamento de Ciencias de la Salud, Universidad Autónoma Metropolitana Iztapalapa, México, D.F., México.|Red Fisiopatología de las Enfermedades Hepáticas, PROMEP-SEP, México D.F., México.
María Concepción
MC
Gutiérrez-Ruiz
D000818:Animals; D002784:Cholesterol / Q000378:metabolism*; D017228:Hepatocyte Growth Factor / Q000502:physiology*; D022781:Hepatocytes / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D019255:NADPH Oxidases / Q000502:physiology*
D017228:Hepatocyte Growth Factor; D002784:Cholesterol; D019255:NADPH Oxidases