Toluene diisocyanate increases vascular endothelial growth factor expression in human bronchial epithelial cells.
- Author:
Hong-juan PENG
1
;
Shao-xi CAI
;
Hai-jin ZHAO
;
Wen-jun LI
;
Wan-cheng TONG
Author Information
- Publication Type:Journal Article
- MeSH: Bronchi; cytology; Cell Line; Cell Survival; Epithelial Cells; drug effects; metabolism; Humans; Protein Isoforms; metabolism; RNA, Messenger; metabolism; Toluene 2,4-Diisocyanate; pharmacology; Vascular Endothelial Growth Factor A; metabolism
- From: Journal of Southern Medical University 2008;28(2):209-212
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of toluene diisocyanate (TDI) on the expression of vascular endothelial growth factor (VEGF) in human bronchial epithelial (HBE) cells.
METHODSTDI-human serum albumin (TDI- HSA) conjugate was prepared using a modified Son's method. MTT assay was used to examine the viability of HBE135-E6E7 cells cultured in serum-free medium after treatment with HSA or TDI-HSA at different concentrations. VEGF mRNA expression of the HBE cells treated with HSA or TDI-HSA at 10, 20, 30 and 40 microg/ ml, respectively, was detected using semi-quantitative RT-PCR.
RESULTSTreatment with 40 microg/ml HSA and 40 microg/ml TDI-HSA did not result in significant changes in the viability of HBE135-E6E7 cells. RT-PCR revealed the constitutive expression of two VEGF isoforms, namely VEGF189 and VEGF165, in cultured HBE135-E6E7 cells. After exposure to TDI-HSA at the different concentrations (except for 10 microg/ml), a significant increase occurred in both VEGF189 and VEGF165 mRNA expressions in HBE135-E6E7 cells as compared with the expressions in the control group and the HSA-treated cells (P<0.05), and significant dose dependence was noted in the effect of TDI-HSA (P<0.05). No significant difference was found in the expressions between the control cells and the HAS-treated cells (P>0.05).
CONCLUSIONTDI induces significant increase in VEGF expression in HBE cells, and VEGF overexpression may play an important role in the pathogenesis of TDI-induced asthma.