A role for Fgl2 (fibroleukin) in thrombophilic-associated human fetal loss has been indicated by previous studies. Clotting of vascular vessels of the placenta and fetus interferes with adequate blood circulation.
The human Fgl2 gene was sequenced with identification of six SNPs, suggesting an association with a population of women suffering from recurrent fetal losses. A small sample size however, prevented precise statistical analyses of this association. In vitro, human endothelial cells (HUVECs) were not found to constitutively express Fgl2, but were shown to up-regulate its expression when challenged with IFN-γ and TNF-α. Interestingly, TNF-α was only shown to induce expression of Fgl2 in HUVECs from male donors and not female donors. A larger case-control study is needed to examine the relationship of Fgl2 with recurrent fetal loss. The role of estrogen in the Th1-induced expression of Fgl2 by HUVECs should also be examined.
