title: Apelin-13 Protects PC12 Cells from Corticosterone-Induced Apoptosis Through PI3K and ERKs Activation.
abstract: It is widely accepted that environmental stress is a risk factor for mental disorders. Glucocorticoid hormones play a vital role in the regulation of physiological response to stress. High concentrations of corticosterone can induce cellular damage in PC12 cells, which possess typical neuronal features. Apelin and its receptor APJ are widely distributed in the central nervous system including limbic structures involved in stress responses. Previous studies have suggested that apelin has a neuroprotective function. However, the effect of apelin on corticosterone-induced neuronal damage remains to be elucidated. In the present study, we explored the potential protective activity of apelin-13 in PC12 cells treated with corticosterone and its underling mechanisms. The viability of the cells, the apoptosis of the cells, the level of phosphorylation of Akt (p-Akt) and extracellular signal-regulated kinases (p-ERKs) and cleaved caspase-3 expression were detected by MTT, Hoechst staining and flow cytometer assays and Western blotting. Results showed that corticosterone induced cells viability loss, cell apoptosis, down-regulation of p-Akt and p-ERKs and up-regulation of cleaved caspase-3. The effects induced by corticosterone were attenuated by apelin-13 pretreatment. Furthermore, apelin-13-mediated anti-viability loss, antiapoptosis and caspase-3 suppression activities were blocked by specific inhibitors of phosphatidylinositol 3-kinase (PI3K) (LY294002) and ERKs (PD98059). The data suggest that apelin-13 protects PC12 cells from corticosterone-induced apoptosis through activating PI3K/Akt and ERKs signaling pathways.
authors.affiliation: Department of Neurology, First Affiliated Hospital, University of South China, Hengyang, 421001, Hunan, People's Republic of China.
authors.forename: Yunjun
authors.initials: Y
authors.lastname: Zou
authors.affiliation: Department of Anesthesiology, First Affiliated Hospital, University of South China, Hengyang, 421001, Hunan, People's Republic of China.
authors.forename: Bo
authors.initials: B
authors.lastname: Wang
authors.affiliation: Department of Neurology, First Affiliated Hospital, University of South China, Hengyang, 421001, Hunan, People's Republic of China.
authors.forename: Wan
authors.initials: W
authors.lastname: Fu
authors.affiliation: Department of Physiology and Institute of Neuroscience, College of Medicine, University of South China, Hengyang, 421001, Hunan, People's Republic of China.
authors.forename: Shouhong
authors.initials: S
authors.lastname: Zhou
authors.affiliation: Department of Neurology, First Affiliated Hospital, University of South China, Hengyang, 421001, Hunan, People's Republic of China. 47089887@126.com.
authors.forename: Yaxiong
authors.initials: Y
authors.lastname: Nie
authors.affiliation: Department of Physiology and Institute of Neuroscience, College of Medicine, University of South China, Hengyang, 421001, Hunan, People's Republic of China. tsw.neuro@126.com.
authors.forename: Shaowen
authors.initials: S
authors.lastname: Tian
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology; D003345:Corticosterone / Q000633:toxicity*; D019610:Cytoprotection / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D004789:Enzyme Activation / Q000187:drug effects / Q000502:physiology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D036341:Intercellular Signaling Peptides and Proteins / Q000494:pharmacology*; D016716:PC12 Cells; D058539:Phosphatidylinositol 3-Kinase / Q000378:metabolism*; D051381:Rats
chemical_list: D036341:Intercellular Signaling Peptides and Proteins; C495199:apelin-13 peptide; D058539:Phosphatidylinositol 3-Kinase; D048049:Extracellular Signal-Regulated MAP Kinases; D003345:Corticosterone
keywords: Apelin; Apoptosis; Corticosterone; ERK; PC12 cells; PI3K