Conclusions
HIF-1α, REDD1 and mTOR may play a significant role in the reaction to hypoxia and oxidative stress and regulate glucose metabolism in the placenta of ICP patients.
Discussion
The placenta from ICP patients is more vulnerable to acute hypoxia and ischemia reperfusion injury. In response to hypoxia stress and oxidative damage in ICP, the placenta activates HIF-1α and REDD1, which in turn may up-regulates glucose transport and anaerobic glycolysis. Conclusions: HIF-1α, REDD1 and mTOR may play a significant role in the reaction to hypoxia and oxidative stress and regulate glucose metabolism in the placenta of ICP patients.
Methods
Placental tissue was collected from 20 women with normal pregnancies and 20 women with ICP. RNA and protein levels of hypoxia inducible transcription factors -1α (HIF-1α), development and DNA protein damage response 1 (REDD1), mammalian target of rapamycin (mTOR), glucose transporter type 1 (GLUT1), phosphoglycerate kinase1 (PGK1) and lacticdehydrogenase (LDHA) in placental tissue were measured by reverse transcriptase real time PCR and Western Blot. Proteins were also located by immunohistochemistry.
Results
Transcript levels were similar for all genes between the two types of placental tissue. In contrast, all protein levels except that of mTOR were significantly higher in placentas from ICP patients than the controls (P < 0.05). All proteins localized to the cytotrophoblast and syncytiotrophoblast.