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BOR - Papers in Press, published online ahead of print February 11, 2004.
Biol Reprod 2004, 10.1095/biolreprod.103.025031
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BIOLOGY OF REPRODUCTION 70, 1822–1827 (2004)
DOI: 10.1095/biolreprod.103.025031
© 2004 by the Society for the Study of Reproduction, Inc.

Pregnancy

Normoxic Induction of the Hypoxic-Inducible Factor-1{alpha} by Interleukin-1ß Involves the Extracellular Signal-Regulated Kinase 1/2 Pathway in Normal Human Cytotrophoblast Cells1

Dong Qian, Hai-Yan Lin, Hong-Mei Wang, Xuan Zhang, Dong-Lin Liu, Qing-Lei Li, and Cheng Zhu2

State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, China

During early pregnancy, an environment of relative low oxygen tension is essential for normal embryonic and placental vasculature. In low-oxygen conditions, the hypoxic-inducible factor-1 (HIF-1), composed of {alpha} and ß subunits, controls the expression of a number of genes such as vascular endothelial growth factor (VEGF), a key angiogenic factor. The recent studies in some tumor cells have found that the labile component, HIF-1{alpha}, is not only activated by hypoxia but also by peptides such as interleukin-1 (IL-1) in normoxia. In this article, we demonstrated that exposure of normal human cytotrophoblast cells to IL-1ß stimulated the expression of HIF-1{alpha} protein. Meanwhile, IL-1ß also induced the secretion of VEGF in normal human cytotrophoblast cells. Our data indicated that IL-1ß induced extracellular signal-regulated kinase (ERK) 1/2 phosphorylation. Moreover, treatment of cells with PD98059, an inhibitor of ERK1/2 signaling, inhibited the stimulation of HIF-1{alpha} protein expression and VEGF secretion by IL-1ß. These data indicate that, in normal human cytotrophoblast cells, IL-1ß induces HIF- 1{alpha}-mediated VEGF secretion and that IL-1ß-stimulated ERK1/2 activation may be involved in this process.

1 Supported by the Special Funds for Major State Basic Research Project (G1999055903), the Knowledge Innovation Project of the Chinese Academy of Sciences (KSCX3-IOZ-07), and the National Natural Science Foundation of China (30200133).

2 Correspondence: Cheng Zhu, State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, 25, Bei Si Huan Xi Lu, Beijing 100080, China. FAX: 86 10 62529248; zhuc{at}panda.ioz.ac.cn




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