Mechanism of JNK signal regulation by placental HSP70 and HSP90 in endothelial cell during preeclampsia

Context: Preeclampsia is a placenta related disorder of during pregnancy resulting in pre- and post-partum complications of the both mother and fetus. It is associated with improper trophoblast invasion and maternal endothelial cell dysfunction leading to a placental dysregulation resulting in premature delivery. Objective: Aim of the present study is to elucidate of the protective role of chaperones (HSP70 and 90) in preeclampsia and to test whether it is associated with oxidative stress level in placental tissue. Materials and methods: Endothelial cell from normotensive and preeclamptic placenta were analyzed for variation in viability and expression of signaling molecules. Results: A significant decrease in viability of endothelial cell (p < 0.05) was noted in preeclamptic samples when compared to normotensive samples. The results indicate that there were increases in HSP70 and HSP90 (p < 0.01), HSF1 (p < 0.01), NF-kB (p < 0.05), JNK1 (p < 0.05), JNK2 (p > 0.05) and Bcl2 (p < 0.05). Discussion: The significant change in the viability of endothelial cell has not predominantly affected the live fetal delivery during preeclampsia. This is governed by alterations in expression of nuclear transcription factors like HSF1, NF-kB and signaling molecules like JNK1/2 and Bcl2 in preeclamptic endothelial cell. Conclusion: This HSP mediated signal changes may contribute to live fetal delivery in spite of existing endothelial cell complication during preeclampsia.