ICEECE2012 Poster Presentations Female Reproduction (99 abstracts)
Chungbuk National University, Cheongju, Republic of Korea.
Introduction: Preeclampsia is a pregnancy-specific disease characterized by 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. The oxidative stress, resulting from deficient remodeling of spiral arteries, is an important inducer of preeclampsia. The potassium-dependent sodium/calcium exchangers including NCKX3 and NCX1 play critical roles in the transport of intracellular calcium that is exchanged with extracellular sodium ions. Calcium related proteins, NCXs, calbindin, calcium pumping proteins (TRPV5-6, PMCA1b) transcripts are abundant in the smooth muscle, uterus, aorta and intestine.
Methods: The expressions of calcium related proteins in the kidney, duodenum and placenta after hypoxic stress in rats at gestation 19.5 day (GD 19.5) was examined by real-time PCR and western blot analysis.
Results: Hypoxic condition did not change fetal weight, however, it significantly increased the weight of placenta compared to normoxic condition. In GD 19.5, renal NCKX3 and TRPV6 expressions were increased, while the levels of NCX1 were decreased in hypoxic rats compared to normoxic pregnant rats. The expressions of CaBP-9k, TRPV5 and PMCA1b were not altered in normoxic- or hypoxic rat tissues. Duodenal expressions of CaBP-9k, TRPV5-6 and PMCA1 were decreased in hypoxic rats, while NCXs were not changed. The transcripts of NCKX3, TRPV5-6 and PMCA1b were highly expressed in the placenta of hypoxic rat.
Conclusions: The expressions of renal, duodenal and placental calcium related proteins appear to be modulated by hypoxia-induced oxidative stress, implying that calcium related proteins may be involved in preeclamptic oxidative stress.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.