Iron is a crucial
element in the human body. Endometrial
iron metabolism is implicated in endometrium receptivity and embryo implantation. Disturbances of the maternal as well as the endometrial
iron homeostasis, such as
iron deficiency, can contribute to the reduced development of the fetus and could cause an increased risk of adverse pregnancy outcomes.
Fractalkine is a unique
chemokine that plays a role in the communication between the mother and the fetus. It has been demonstrated that FKN is involved in the development of endometrial receptivity and embryo implantation, and it functions as a regulator of
iron metabolism. In the present study, we examined the effect of FKN on the
iron metabolism of HEC-1A endometrial cells in a state of
iron deficiency mediated by
desferrioxamine treatment. Based on the findings, FKN enhances the expression of
iron metabolism-related genes in
iron deficiency and modifies the
iron uptake via
transferrin receptor 1 and
divalent metal transporter-1, and
iron release via
ferroportin. FKN can activate the release of
iron from
heme-containing
proteins by elevating the level of
heme oxygenase-1, contributing to the redistribution of intracellular
iron content. It was revealed that the endometrium cells express both mitoferrin-1 and 2 and that their levels are not dependent on the
iron availability of the cells. FKN may also contribute to maintaining mitochondrial
iron homeostasis. FKN can improve the deteriorating effect of
iron deficiency in HEC-1A endometrium cells, which may contribute to the development of receptivity and/or provide
iron delivery towards the embryo.