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Hypoxia-mediated down-regulation of OCTN2 and PPARα expression in human placentas and in BeWo cells
Ting-Ting Chang1, Ming-Kwang Shyu, Min-Chuan Huang
1School of Pharmacy, College of Medicine, National Taiwan University, Taipei 100, Taiwan.
The objective of the present study was to investigate the effects of hypoxia on placental expression of OCTN2 and PPARα. OCTN2 and PPARα expression in the human placenta in the presence or absence of preeclampsia was examined by immunohistochemical (IHC) analysis, Western blotting, and quantitative polymerase chain reaction (qPCR). Effects of hypoxia on the expression of OCTN2 and PPARα in human placental explants and human choriocarcinoma BeWo cells were examined by Western blotting and qPCR analyses. IHC, Western blot, and qPCR studies showed that OCTN2 and PPARα protein and mRNA levels were lower in syncytiotrophoblasts from preeclamptic human placentas than in those from normal placentas. Hypoxic treatment caused a decrease in OCTN2 and PPARα expression in human placental explants and in BeWo cells. WY14643, a PPARα agonist, caused an increase in OCTN2 expression in BeWo cells under hypoxic conditions. In conclusion, under hypoxic conditions, placental OCTN2 is down-regulated through PPARα-mediated pathways.
The objective of the present study was to investigate the effects of hypoxia on placental expression of OCTN2 and PPARα. OCTN2 and PPARα expression in the human placenta in the presence or absence of preeclampsia was examined by immunohistochemical (IHC) analysis, Western blotting, and quantitative polymerase chain reaction (qPCR). Effects of hypoxia on the expression of OCTN2 and PPARα in human placental explants and human choriocarcinoma BeWo cells were examined by Western blotting and qPCR analyses. IHC, Western blot, and qPCR studies showed that OCTN2 and PPARα protein and mRNA levels were lower in syncytiotrophoblasts from preeclamptic human placentas than in those from normal placentas. Hypoxic treatment caused a decrease in OCTN2 and PPARα expression in human placental explants and in BeWo cells. WY14643, a PPARα agonist, caused an increase in OCTN2 expression in BeWo cells under hypoxic conditions. In conclusion, under hypoxic conditions, placental OCTN2 is down-regulated through PPARα-mediated pathways.
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