Korean J Obstet Gynecol.
2001 May;44(5):957-963.
Effects of Th1 type cytokines on secretion of vascular endothelial growth factor by human first trimester trophoblast cell line
- Affiliations
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- 1Department of Obstetrics and Gynecology, Yonsei University, Wonju College of Medicine, Wonju, Kangwon-do, Korea.
- 2Department of Microbiology, Yonsei University, Wonju College of Medicine, Wonju, Kangwon-do, Korea.
- 3Department of Institute of Basic Medical Science, Yonsei University, Wonju College of Medicine, Wonju, Kangwon-do, Korea.
Abstract
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Embryo implantation and development are critically dependent upon the regulation of
angiogenesis and adequate immunologic acceptance. These local angiogenesis and vascular
permeability are regulated by the interaction between fetal trophoblast, uterine decidua,
and endothelial cells through the key mediator, vascular endothelial growth factor (VEGF).
PROBLEM: The mechanism through which VEGF regulation occurs at the feto-maternal interface is
poorly understood. The Th1 type cytokines are known to be harmful to the successful maintenance of early
pregnancy at the feto-maternal interface.
OBJECTIVE
To clarify whether the Th1 type cytokines could be involved in the regulation of VEGF
secretion at the feto-maternal interface.
Method of Study : we investigated the effects of Th1 type cytokines on VEGF secretion in human first
trimester trophoblast cell-line by using reverse transcription polymerase chain reaction(RT-PCR)and
enzyme-linked immunosorbent assay (ELISA).
RESULTS
The trophoblast cells expressed VEGF constitutively and the main isoforms were VEGF121
and VEGF165. When cultured in the presence of IFN-gamma or IL-2, VEGF secretion was most significantly
increased by IFN-gamma treatment but not affected by IL-2 treatment. The level of intracellular VEGF was also
increased by IFN-gamma treatment.
CONCLUSION
These results suggest that IFN-gamma, despite of harmful Th1 type cytokine to the maint
enance of early pregnancy, may regulate the production of VEGF in early gestational trophoblasts.