title: Fibroblast growth factor 21 as a possible endogenous factor inhibits apoptosis in cardiac endothelial cells.
abstract: BACKGROUND
  Fibroblast growth factor 21 (FGF21) is a new member of FGF super family that is an important endogenous regulator for systemic glucose and lipid metabolism. This study aimed to explore whether FGF21 reduces atherosclerotic injury and prevents endothelial dysfunction as an independent protection factor.
  
  
  METHODS
  The present study was designed to investigate the changes of FGF21 levels induced by oxidized-low density lipoprotein (ox-LDL), and the changes of apoptosis affected by regulating FGF21 expression. The FGF21 mRNA levels of cultured cardiac microvascular endothelial cells (CMECs) were determined by real time-PCR and the protein concentration in culture media was detected by enzyme-linked immunosorbent assay. We analyzed the different expression levels of untreated controls and CMECs incubated with ox-LDL, and the changes of CMECs apoptosis initiated by the enhancement or suppression of FGF21 levels.
  
  
  RESULTS
  The secretion levels of FGF21 mRNA and protein were significantly upregulated in CMECs incubated with ox-LDL. Furthermore, FGF21 levels increased by 200 µmol/L bezafibrate could reduce CMECs apoptosis, and inhibit FGF21 expression by shRNA induced apoptosis (P < 0.05).
  
  
  CONCLUSIONS
  FGF21 may be a signal of injured target tissue, and may play physiological roles in improving the endothelial function at an early stage of atherosclerosis and in stopping the development of coronary heart disease.
authors.affiliation: Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Lü
authors.forename: Jing-Hua
authors.initials: JH
authors.lastname: Liu
authors.forename: Li-Ke
authors.initials: LK
authors.lastname: Zhang
authors.forename: Jie
authors.initials: J
authors.lastname: DU
authors.forename: Xiang-Jun
authors.initials: XJ
authors.lastname: Zeng
authors.forename: Gang
authors.initials: G
authors.lastname: Hao
authors.forename: Ji
authors.initials: J
authors.lastname: Huang
authors.forename: Dong-Hui
authors.initials: DH
authors.lastname: Zhao
authors.forename: Guo-Zhong
authors.initials: GZ
authors.lastname: Wang
authors.forename: Ying-Chuan
authors.initials: YC
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis; D001629:Bezafibrate / Q000494:pharmacology; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000517:prevention & control*; D042783:Endothelial Cells / Q000502:physiology*; D005346:Fibroblast Growth Factors / Q000032:analysis / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000633:toxicity; D008297:Male; D047493:PPAR alpha / Q000502:physiology; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar
chemical_list: D008077:Lipoproteins, LDL; D047493:PPAR alpha; D012333:RNA, Messenger; C414620:fibroblast growth factor 21; C099252:oxidized low density lipoprotein; D005346:Fibroblast Growth Factors; D001629:Bezafibrate