Hydrogen dioxide increases the expression of vascular endothelial growth factor in human bronchiolar epithelium cell via a PI3K-dependent pathway.
- Author:
Xiang-bo SHEN
1
;
Hai-jin ZHAO
;
Shao-xi CAI
;
Hong-juan PENG
;
Wen-jun LI
;
Wan-cheng TONG
Author Information
- Publication Type:Journal Article
- MeSH: Actins; metabolism; Bronchi; cytology; Cell Line; Epithelial Cells; cytology; metabolism; Humans; Hydrogen Peroxide; pharmacology; Oxidative Stress; physiology; Phosphatidylinositol 3-Kinases; metabolism; Signal Transduction; Vascular Endothelial Growth Factor A; genetics; metabolism
- From: Journal of Southern Medical University 2010;30(2):228-231
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of hydrogen dioxide (H(2)O(2)) on the expression of vascular endothelial growth factor (VEGF) in human bronchiolar epithelial (HBE) cells.
METHODSMTT assay was used to assess HBE cell viability after exposure to different concentrations of H(2)O(2). VEGF/beta-actin gene fragments were amplified simultaneously by RT-PCR from the total HBE cell RNA, and VEGF protein expression in the cells was detected using ELISA.
RESULTSThe exposure to 200 micromol/L H(2)O(2) did not obviously affected the cell viability. Compared with those in the control cell, VEGF165/beta-actin and VEGF189/beta-actin ratios were significantly increased in the cells after treatment with 50, 200, and 600 micromol/L H(2)O(2) (P<0.05). The protein expression of VEGF significantly increased after 50 micromol/L H(2)O(2) treatment (P<0.05), but significantly decreased with pretreatment with the PI3K inhibitor Ly294002 (P>0.05).
CONCLUSIONOxidative stress increases the expression of VEGF via a PI3K-dependent pathway in human bronchiolar epithelial cells, which may play an important role in the onset and maintenance of chronic inflammation in asthma.
