RT Journal Article SR Electronic T1 sFlt-1 (sVEGFR1) induces placental endoplasmic reticulum stress in trophoblast cell: implications for the complications in preeclampsia- an in vitro study JF bioRxiv FD Cold Spring Harbor Laboratory SP 240481 DO 10.1101/240481 A1 Sankat Mochan A1 Manoj Kumar Dhingra A1 Betsy Varghese A1 Sunil Kumar Gupta A1 Shobhit saxena A1 Pallavi Arora A1 Neerja Rani A1 Arundhati Sharma A1 Kalpana Luthra A1 Sadanand Dwivedi A1 Neerja Bhatla A1 Rani Kumar A1 Renu Dhingra YR 2017 UL http://biorxiv.org/content/early/2017/12/28/240481.abstract AB Background The concentration of sFlt-1, a major anti-angiogenic protein in maternal circulation has been seen to be raised in preeclamptic pregnancies. Endoplasmic reticulum (ER) stress represents one of the three (immunological, oxidative and ER stress) major stresses which placenta undergoes during pregnancies. The present study is designed to investigate the role of sFlt-1 in induction of ER stress in trophoblast cells.Materials and Methods Maternal serum levels of anti-angiogenic protein sFlt-1 and central regulator of unfolded protein response GRP78 was measured using sandwich ELISA. The expression of various ER stress markers (GRP78, eIF2α, XBP1, ATF6 and apoptotic protein CHOP) were analyzed depending on various treatments given to the trophoblast cells using Immunofluorescence, western blot and q-RT PCR.Results Increased expression of ER stress markers (GRP78, eIF2α, XBP1 ATF6 and apoptotic protein CHOP) was detected in the placental trophoblast cells treated with raised concentration of sFlt-1.Conclusion Significant upregulated expression of ER stress markers in trophoblast cells exposed with increased concentration of sFlt-1 suggested that it may be one of the anti-angiogenic factors present in maternal sera which not only contributes to oxidative stress but also may cause endoplasmic reticulum stress.