Endoplasmic reticulum (ER) homeostasis is cycle-dependent and the inflammatory cytokines TNF-α and ILI-1β induce er stress by regulating BIP expression in human endometrial ENDOTHELIAL CELLS

Abstract

Endoplasmic reticulum (ER) homeostasis must be controlled for normal protein synthesis and transition through the ER otherwise ER stress elicits a signaling cascade known as the unfolded protein response (UPR), which influences both life and death decisions in cells. BIP/GRP78 is a 78-kDa glucose regulated protein centrally involved in regulation of ER stress. Inflammatory cytokines TNF-alpha (TNF-α) and IL-1beta (IL-1β) are shown to agitate ER homeostasis through affecting BIP activity. Our hypothesis is that BIP expression human endometrial endothelial cells (HEECs) are controlled in a menstrual cycle dependent manner and that TNF-α and IL-1β disrupt the ER homeostasis by modulating BIP activity in HEEC.