Expression of Vascular Endothelial Growth Factor mRNA in Endotoxin Induced Otitis Media with Effusion of the Rat.
- Author:
Myung Won KIM
1
;
Hak Hyun JUNG
;
Baik Ahm CHANG
;
Sang Cheol LEE
;
Eun Seok KIM
;
Hyun Ho LIM
Author Information
1. Department of Otolaryngology, Seoul Adventist Hospital, Seoul, Korea. hakjung@netsgo.com
- Publication Type:Original Article
- Keywords:
Vascular endothelial growth factor;
Otitis media;
Vascular permeability;
PCR;
Rat
- MeSH:
Animals;
Capillary Permeability;
Ear, Middle;
Endothelial Cells;
Heparin;
Mucous Membrane;
Otitis Media with Effusion*;
Otitis Media*;
Otitis*;
Polymerase Chain Reaction;
Rats*;
RNA, Messenger*;
Vascular Endothelial Growth Factor A*
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
1999;42(5):559-564
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: The vascular endothelial growth factor (VEGF), a heparin binding growth factor specific for endothelial cells, is both a potent enhancer of vascular permeability and an angiogenic growth factor. The purpose of this study was to investigate the semi-quantitative expression levels of multiple VEGF mRNA splicing variants in endotoxin-induced otitis media with effusion (OME) of rat. MATERIALS AND METHODS: We instilled endotoxin and saline as a control into the middle ear cavity of the rat, and middle ear mucosa were taken at 0 h, 1 h, 3 h, 6 h, 12 h, 1 d, 3 d, 7 d, and 14 d. The levels of splicing variants of VEGF transcripts were evaluated by semi-quantitative RT-PCR. RESULTS: Expression of VEGF164 mRNA and VEGF120 mRNA was first identified at 1 h after endotoxin instillation and was dramatically increased between 6 h and day 1 and then progressively decreased by day 7. Expression level of VEGF120 mRNA was 1.34+/-0.27 fold higher than that of VEGF164, and the expression level of VEGF164 was 3.89+/-0.97 fold higher than that of VEGF188. CONCLUSION: These results suggest that VEGF may be primarily responsible for the increased vascular permeability in OME and that it seems to play a significant role in the pathogenesis of OME.
