title: Protective role and related mechanism of Gnaq in neural cells damaged by oxidative stress.
abstract: Gnaq is a member of G protein family and is rich in brain tissue. It has attracted the attention of many researchers in melanoma due to its high ratio of mutation. We have previously reported that the expression level of Gnaq in the mouse forebrain cortex was significantly decreased with age. Oxidative stress (OS) is the main cause leading to brain aging and related diseases. The roles and mechanisms of Gnaq in antioxidation in the brain have not been fully explored. In the present study, gene recombinant technique and lentivirus transfection technique were used to generate a Gnaq-overexpression cell model (Gnaq-SY5Y) coupled with H2O2 to build an OS model. The viability of cells, concentration of reactive oxygen species (ROS), apoptosis-related proteins (Bcl-2 and Bax), and signal pathways (NF-κB and Erk1/2) were compared between model cells and control cells. Results showed that the antioxidative ability of Gnaq-SY5Y cells was significantly improved. Concomitantly, the ROS level in Gnaq-SY5Y cells was significantly decreased whether the cells were subject to or not to H2O2 treatment. Anti-apoptotic protein Bcl-2 was up-regulated and apoptosis-promoting protein Bax was down-regulated in Gnaq-SY5Y cells after treatment with H2O2. NF-κB and phosphorylated Erk1/2 (p-Erk1/2) was significantly down-regulated in Gnaq-SY5Y cells. H2O2 treatment decreased Gnaq expression but increased NF-κB and p-Erk1/2 expressions in Gnaq-SY5Y cells. It is therefore concluded that Gnaq plays a pivotal role in antioxidation in neural cells. A possible mechanism for this would be that the overexpressed Gnaq inhibits the cellular damaging effect mediated by NF-κB and Erk1/2 signal pathways.
authors.affiliation: Department of Anatomy and Histoembryology, Kunming Medical University, Kunming 650500, China.
authors.forename: Nannan
authors.initials: N
authors.lastname: Jia
authors.affiliation: Department of Head and Neck Surgery, Third Affiliate Hospital, Kunming Medical University, Kunming 650118, China.
authors.forename: Guoping
authors.initials: G
authors.lastname: Li
authors.affiliation: Department of Anatomy and Histoembryology, Kunming Medical University, Kunming 650500, China.
authors.forename: Pu
authors.initials: P
authors.lastname: Huang
authors.affiliation: Biomedical Engineering Research Center, Kunming Medical University, Kunming 650500, China.
authors.forename: Jiazhi
authors.initials: J
authors.lastname: Guo
authors.affiliation: Department of Rehabilitation, Second People's Hospital of Kunming, Kunming 650500, China.
authors.forename: Lugang
authors.initials: L
authors.lastname: Wei
authors.affiliation: Biomedical Engineering Research Center, Kunming Medical University, Kunming 650500, China.
authors.forename: Di
authors.initials: D
authors.lastname: Lu
authors.affiliation: Department of Anatomy and Histoembryology, Kunming Medical University, Kunming 650500, China.|International Education School, Kunming Medical University, Kunming 650500, China.
authors.forename: Shaochun
authors.initials: S
authors.lastname: Chen
mesh_terms: D017209:Apoptosis / Q000502:physiology; D002460:Cell Line; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000378:metabolism*; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology*; D016328:NF-kappa B / Q000378:metabolism*; D009474:Neurons / Q000166:cytology* / Q000502:physiology*; D000066829:Neuroprotection / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species
chemical_list: C554061:GNAQ protein, human; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D043802:GTP-Binding Protein alpha Subunits, Gq-G11
keywords: Gnaq; SY5Y cell line; antioxidation; overexpression; oxidative stress