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Submitted on April 29, 2004
Accepted on October 22, 2004
Division of High Risk Pregnancy, Department of Obstetrics and Gynecology, and Department of Medical Research, Mackay Memorial Hospital, Taipei, Taiwan; Mackay Medicine, Nursing and Management College, Taipei, Taiwan; Academic Unit of Obstetrics and Gynaecology, Medical School, University of Manchester, UK
* To whom correspondence should be addressed.
John D. Aplin, E-mail: John.Aplin{at}man.ac.uk
Villous fibrosis is associated with oxygen deprivation in placental pathology, but the signaling networks and growth factors involved in activating the relevant cellular repair mechanisms are largely unknown. Transforming growth factor (TGF) is a powerful enhancer of extracellular matrix (ECM) production as well as an important immune suppressor that has been linked with fibrosis in several tissues. Here cell culture methods were used to investigate possible links between hypoxia, elevated TGF
-1 and altered ECM production in placenta. Term placental fibroblasts were isolated and cultured under hypoxia (3% O2) or in the presence of TGF-1, and the expression of fibronectin, collagen I and collagen IV was examined using immunohistochemistry, enzyme-linked immunosorbant assay (ELISA) of cell monolayers with associated ECM, and real-time RT-PCR. The effect of hypoxia on endogenous production of TGF-1,2 and 3 was also examined. Both TGF-1 and hypoxia increased fibronectin, collagen I, and collagen IV protein and mRNA in placental fibroblasts. However, TGF-1-3 production was not increased by culturing the cells under hypoxic conditions for 5 days. Thus, increased ECM expression under hypoxia was not mediated directly by increased TGF-. We conclude that ECM production can be stimulated independently by hypoxia and TGF-1.
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