In vitro Hypoxia-Reoxygenation as a Model to Study Endoplasmic Reticulum Stress-Related Apoptosis in the Human Placenta

Project: National Science and Technology CouncilNational Science and Technology Council Academic Grants

Project Details


The endoplasmic reticulum (ER) is the cellular site for Ca2+ storage and for synthesis, folding, and maturation of most secreted and transmembrane proteins. ER stress occurs when there is an imbalance between the cellular demand for ER function and ER capacity. There is increasing evidence suggesting that ER stress is associated with a range of diseases, including ischemia/reperfusion injury and pregnancy complications such as intrauterine growth restriction (IUGR). Our previous work shows that hypoxia-­‐reoxygenation (HR) is a possible mechanism for placental oxidative stress in preeclampsia and IUGR. Here we will apply this model to induce ER stress and investigate possible mechanisms for ER stress-­‐related apoptosis in cytotrophoblasts. Cytotrophoblast cells will be obtained from normal term placentas and used to study the changes of Bcl-­‐2 family proteins and Ca2+ homeostasis in ER and activation of the Ire1/TRAF2/Ask1 signaling pathway. We will also compare the levels of ER stress between placentas from pregnancy complicated by IUGR and those from normal pregnancy. The results will extend our understanding of the role of ER stress in trophoblast cell death.

Project IDs

Project ID:PC10007-1193
External Project ID:NSC100-2314-B182A-082-MY3
Effective start/end date01/08/1131/07/12


  • placenta


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