Impact of Axis of GHRH and GHRH Receptor on Cell Viability and Apoptosis of the Placental Choriocarcinoma Cell Line.

The expression of GHRH-R is significantly lower in placental tissues from early pregnancy loss compared to normal controls. Inhibition of GHRH-R with the antagonist JMR-132 in JEG-3 cells reduces cell viability and induces apoptosis through activation of caspase-3, p38, and p53 pathways, and by increasing ER stress markers such as GRP78 and phospho-eIF2α while inhibiting Akt phosphorylation.

The study measured GHRH-R expression in human placental villous tissues and JEG-3 placental choriocarcinoma cells. It then treated JEG-3 cells with the GHRH antagonist JMR-132 and assessed effects on cell viability, apoptosis, and related signaling pathways using molecular assays. Additional experiments involved pretreatment with salubrinal and GHRH-R knockdown to confirm pathway involvement.

Understanding how GHRH-R regulates placental cell survival and death could reveal targets for treating placental dysfunction and related pregnancy complications. It also advances knowledge of peptide hormone signaling in placental development.

The study used a placental cancer cell line (JEG-3), which may not fully represent normal placental cells. The exact clinical implications for pregnancy loss require further validation in vivo and in human subjects.