What is it about?
The actions of THs are highly pleiotropic, affecting many tissues at different developmental stages. As a consequence, their effects on proliferation and differentiation are highly heterogeneous depending on the cell type, the cellular context, and the developmental or transformation status. Maternal THs are important in promoting normal fetal development especially the placental and CNS development. Clinical epidemiological and basic findings clearly show that maintaining normal TH regulation from the beginning of pregnancy is important to reduce the risk of obstetric complications and to ensure optimal neurodevelopment of the offspring. In normal pregnancy, transplacental TH passage is modulated by plasma membrane THTs, Ds, sulfotransferases, TRs and several different proteins within placental cells. In pathological/abnormal pregnancies with either maternal or fetal THs disturbances (hypoor hyper-thyroidism), the placenta lacks the full compensatory mechanisms necessary to optimize the maternal–fetal transfer of THs to achieve the normality of TH levels in the fetus.
Featured Image
Why is it important?
The actions of THs are highly pleiotropic, affecting many tissues at different developmental stages. As a consequence, their effects on proliferation and differentiation are highly heterogeneous depending on the cell type, the cellular context, and the developmental or transformation status. Maternal THs are important in promoting normal fetal development especially the placental and CNS development. Clinical epidemiological and basic findings clearly show that maintaining normal TH regulation from the beginning of pregnancy is important to reduce the risk of obstetric complications and to ensure optimal neurodevelopment of the offspring. In normal pregnancy, transplacental TH passage is modulated by plasma membrane THTs, Ds, sulfotransferases, TRs and several different proteins within placental cells. In pathological/abnormal pregnancies with either maternal or fetal THs disturbances (hypoor hyper-thyroidism), the placenta lacks the full compensatory mechanisms necessary to optimize the maternal–fetal transfer of THs to achieve the normality of TH levels in the fetus.
Perspectives
Further studies are still needed to improve our understanding of the mechanisms mediating the transplacental transport of THs in both human and animals, particularly the role of the different THTs, and the mechanisms that ensure that sufficient amounts of THs are protected from D3 inactivation during their transit across the placenta. Such knowledge would facilitate the development of interventions to increase TH passage in pathological situations, in order to ensure normal fetal development. A better understanding of these mechanisms would also permit us to refine the timing and dosage of the increase in levothyroxine therapy in hypothyroid pregnant women and to establish whether thyroxine on its own is indeed the best form of TH replacement in pregnancy. Elucidation of tissue-, cell-, and sex-specific expression of individual Ds and THTs during the development of both human and animals, in the adult, during aging and when sick. I hope that new insights into the complex actions by which the THs and their receptors control cell proliferation and differentiation will be provided in the near future.
Full Professor Ahmed R. G.
Division of Anatomy and Embryology, Zoology department, Faculty of Science, Beni-Suef University, Egypt.
Read the Original
This page is a summary of: Thyroid Hormone, July 2012, IntechOpen,
DOI: 10.5772/2964.
You can read the full text:
Contributors
The following have contributed to this page
