title: Proteomic study on the protective mechanism of fibroblast growth factor 21 to ischemia-reperfusion injury.
abstract: Fibroblast growth factor (FGF)-21 is a novel regulator of insulin-independent glucose transport in 3T3-L1 adipocytes and has glucose and triglyceride lowering effects in rodent models of diabetes. In this study, we found that FGF-21 can significantly attenuate ischemia-reperfusion (I/R) induced damage in H9c2 cells (rat heart). However, it is unclear which signal transduction pathway is involved in the cardioprotective effect of FGF-21. Thus, this study was designed to investigate the potential mechanism induced by FGF-21. The results showed that FGF-21 treatment prevented the oxidative stress and apoptosis associated with I/R damage by reducing the levels of superoxide anions, inhibiting glycogen synthase kinase (GSK) 3β by activating Akt phosphorylation, and recovering the levels of ATP synthase pyruvate kinase isozymes M1 and protein kinase C, thereby improving energy supply. In summary, we conclude that FGF-21 protects H9c2 cells against I/R injury mainly through the Akt-GSK-3β-caspase-3 dependent pathway, preventing oxidative stress, and recovery of the energy supply.
authors.affiliation: a Zhejiang Provincial Key Laboratory of Biopharmaceuticals, Wenzhou Medical College, Wenzhou, Zhejiang 325035, P.R. China.
authors.forename: Wei-Tao
authors.initials: WT
authors.lastname: Cong
authors.forename: Jin
authors.initials: J
authors.lastname: Ling
authors.forename: Hai-Shan
authors.initials: HS
authors.lastname: Tian
authors.forename: Ren
authors.initials: R
authors.lastname: Ling
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
authors.forename: Bin-Bin
authors.initials: BB
authors.lastname: Huang
authors.forename: Ting
authors.initials: T
authors.lastname: Zhao
authors.forename: Yuan-Meng
authors.initials: YM
authors.lastname: Duan
authors.forename: Li-Tai
authors.initials: LT
authors.lastname: Jin
authors.forename: Xiao Kun
authors.initials: XK
authors.lastname: Li
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002316:Cardiotonic Agents; D053148:Caspase 3 / Q000502:physiology; D002452:Cell Count; D002460:Cell Line; D002851:Chromatography, High Pressure Liquid; D016000:Cluster Analysis; D004591:Electrophoresis, Polyacrylamide Gel; D004996:Ethidium; D005346:Fibroblast Growth Factors / Q000494:pharmacology*; D038362:Glycogen Synthase Kinase 3 / Q000502:physiology; D006801:Humans; D032383:Myocytes, Cardiac / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D040901:Proteomics; D051057:Proto-Oncogene Proteins c-akt / Q000502:physiology; D060888:Real-Time Polymerase Chain Reaction; D015427:Reperfusion Injury / Q000188:drug therapy*; D015398:Signal Transduction / Q000187:drug effects; D012844:Sincalide / Q000378:metabolism; D021241:Spectrometry, Mass, Electrospray Ionization
chemical_list: D002316:Cardiotonic Agents; C414620:fibroblast growth factor 21; D005346:Fibroblast Growth Factors; D051057:Proto-Oncogene Proteins c-akt; D038362:Glycogen Synthase Kinase 3; D053148:Caspase 3; D004996:Ethidium; D012844:Sincalide