Abstract
Preeclampsia is pregnancy-specific disease characterized de-novo development of concurrent hypertension, proteinuria and oxidative stress in placenta. Hypoxia occurs during the development of placenta in the first trimester and is implicated in trophoblast differentiation. In placenta, intervillous blood flow increases after 10 weeks of gestation and results in exposure of trophoblast cells to oxygen. During last trimester of gestation, the calcium (Ca2+) transport from mother to fetus increases dramatically in response to the accelerated demand for Ca2+ caused by bone mineralization in the fetus. Regarding the molecular basis of Ca2+ transport, several studies suggest that transcellular active Ca2+ transport is comprised of three processes: (1) the apical Ca2+ entry, (2) the binding with calbindins that serves as an intracellular Ca2+ buffer, and (3) basolateral exit. In this study, cell membrane and cytosolic calcium transporters (TRPV6, PMCA1, NCKX3 and CaBP-28k) were investigated at induced oxidative stress in human placental cell line (BeWo). The expression of calcium transporters (TRPV6, PMCA1, NCKX3 and CaBP-28k) were potential roles in BeWo cell remain to be clarified. In hypoxia, human placental cell (BeWo) expression of TRPV6 mRNA and protein level was not altered, however, calcium transporters (NCKX3, CaBP-28k) were increase at hypoxic BeWo cell compared with control group (normoxia). In addition, expression of PMCA1 mRNA and protein was decreased at hypoxic BeWo cell. Taken together, these results indicate that calcium transporters (TRPV6, PMCA1, NCKX3 and CaBP-28k) are distinctly expressed by induced oxidative stress, in BeWo cell, suggesting that alterations of calcium transporters in hypoxic stress may be involved in placenta cell is a determinant factor affecting calcium transfer in BeWo cell model. (poster)
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