The effect of ginsenoside Rk1 in junctional protein of severe preeclamptic placenta / 대한산부인과학회지

OBJECTIVE: To investigate the differential expression of junctional proteins in the normal and preeclamptic human placenta and the effect of ginsenoside Rk1 in junctional proteins. METHODS: Placental tissues from 10 women with severe preeclampsia and 5 normal women were collected at the time of their cesarean section. Five of 10 preeclamptic women were complicated with intrauterine growth restriction (IUGR). Immunohistochemistry and Western blotting was employed to localize junctional proteins (zo-1, occludin and plakoglobin) positive cells. The placental explant culture was performed to investigate if Rk1 can attenuate the expression of junctional proteins (zo-1, occluding and plakoglobin) induced by deferoxamine-induced hypoxia. Rk1 was treated at the day 3 and Western blot analysis was performed for protein quantification. RESULTS: There was no different expression of zo-1 and plakoglobin among all the study groups. Occludin showed negative at the endothelial cells of the terminal villi in both normal and preeclampsia groups. At the endothelial cells of the stem villi, occludin was detected in both normal and severe preeclamptic placenta with normal fetal growth. However, severe preeclampsia with IUGR were decreased expression of occludin at the endothelial cells of the stem villi. When we administered Rk1 to the placenta treated with DFO, expression of occludin was not different. CONCLUSION: The placental expression of zo-1 and plakoglobin were not different among the study groups, while that of occludin was significantly decreased at the endothelium of stem villi in severe preeclampsia with IUGR. Rk-1 showed no effect on the placental junctional proteins. These results suggest that occludin may play a role in pathophysiology of fetal growth restriction in utero.

Differential expression of adenosine receptors in normal and preeclamptic human placentas / 대한산부인과학회지

OBJECTIVE: The aim of the study was to investigate the differential expression of adenosine receptors (ADORs) in the normal and preeclamptic placenta. METHODS: Placentas were obtained from women undergoing cesarean section with normal and preeclamptic pregnancies at term. Total RNA was reverse transcribed using ADORs gene specific primers. RT-PCR measurements were made semi-quantitatively. Western blot analysis was performed for protein quantitation. Immunohistochemical staining with anti-adenosine receptor antibodies were employed to localize adenosine receptors in placental tissues. RESULTS: RT-PCR revealed that A2aR, A2bR, and A3R mRNA, not A1 receptor mRNA were expressed in both normal and preeclamptic placenta. Interestingly, there were somewhat higher expressions of A2aR, A2bR, and A3R mRNA in preeclamptic placenta than in normal placenta. Western blotting revealed that A2a, A2b, and A3 receptors were all present in the placental tissue as verified by immunoreactive protein bands. The bands for the A2a, A2b, and A3 receptors were stronger in preeclamptic placenta than in normal placenta. A2a and A2b receptors were detected in endothelial cell, whereas we could not find the staining for A3 receptor in endothelial cells. Importantly, A3 antibody had high intensity of staining in trophoblasts in preeclampsia. CONCLUSION: To our knowledge, this study is the first to evaluate the expression of ADORs in normal placenta, and to compare ADOR subtypes in normal versus preeclamptic placenta. This study suggests that the specific subtype of ADORs may have a role in the development of preeclampsia.