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Fibroblast growth factor 21 as a possible endogenous factor inhibits apoptosis in cardiac endothelial cells.

Authors: Lu, Y  Liu, JH  Zhang, LK  Du, J  Zeng, XJ  Hao, G  Huang, J  Zhao, DH  Wang, GZ  Zhang, YC 
Citation: Lu Y, etal., Chin Med J (Engl). 2010 Dec;123(23):3417-21.
Pubmed: (View Article at PubMed) PMID:22166524

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 micromol/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.


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CRRD Object Information
CRRD ID: 10401877
Created: 2015-10-09
Species: All species
Last Modified: 2015-10-09
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.