The identification of relaxin-binding on the amnion epithelial cells, syncytiotrophoblast, blood vessels and stromal cells within the term placenta is consistent with Bryant-Greenwood and coworkers’ hypothesis that decidual and/ or placental relaxin acts locally via autocrine and/or paracrine mechanisms. The binding of decidual and/or placental relaxin to the amnion epithelial cells and stromal cells may contribute to connective tissue remodeling at the maternal-fetal interface during late pregnancy and at birth.
The physiological significance of relaxin binding to syncytiotrophoblasts is more speculative. Relaxin might control the production of proteins such as follistatin, transforming growth factor, and interleukin-1, which in turn regulate hCG production. Relaxin may also modulate the transfer of substances between the mother and fetus via autocrine regulation of transport mechanisms such as the glucose transport protein-1, which is localized on the syncytiotrophoblasts of the human placenta and increases as pregnancy progresses. As in the reproductive tract, unpublished results), the binding of relaxin to the placental blood vessels may cause their dilation and thereby contribute to maintenance of adequate blood supply to the fetus. antibiotic levaquin
Our previous studies with pigs and rats demonstrated that endogenous circulating relaxin does not occupy relaxin-binding sites to the extent that it interferes noticeably with binding of the biotinylated relaxin in reproductive and other tissues.