Journal
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
Volume 189, Issue 2, Pages 583-588Publisher
MOSBY, INC
DOI: 10.1067/S0002-9378(03)00538-6
Keywords
ASCT2; BeWo cells; hypoxia; placenta; syncytin
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OBJECTIVE: The purpose of this study was to test the hypothesis that hypoxia down-regulates placental syncytin, which could play a role in altered placentogenesis; we investigated the influence of hypoxia on syncytin and its receptor ASCT2 gene expression in BeWo cells and in ex vivo perfused human cotyledons. STUDY DESIGN: BeWo cells were incubated with deferoxamine or cobalt chloride under normoxia and hypoxia. Additionally, a model of dually ex vivo perfused cotyledons was applied. Under hypoxic and cobalt chloride stimuli syncytin, ASCT2, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), b-actin, and b(2)(2)(- microglobulin (b)-MG) messenger RNAs were analyzed with the use of real-time polymerase chain reaction. RESULTS: Hypoxia, deferoxamine, and cobalt chloride markedly decreased syncytin messenger RNA in BeWo cells, whereas ASCT2 messenger RNA was not altered significantly. In isolated perfused cotyledons, hypoxia also reduced syncytin (P < .05) but not ASCT2 messenger RNA. CONCLUSION: Our data provide first evidence that syncytin gene expression is down-regulated by hypoxia, which strengthens the hypothesis that syncytin is reduced in disturbed pregnancies in the course of placental hypoxia.
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