Short-term effects of thyroid hormones during development: Focus on signal transduction

Membrane-initiated actions of thyroid hormones on the male reproductive system

“…Also, the nongenomic responses typically have a time-course of seconds or minutes and are frequently associated with secondary messenger and kinase signaling pathways (Scapin et al, 2010). Moreover, it is widely demonstrated that membrane-initiated rapid responses to thyroid hormones include alterations in ionic fluxes and in membrane potentials (Incerpi et al, 1999;Davis et al, 2010).…”

“…Although the mechanism of action of thyroid hormones has been classically established as a genomic action, it has been largely described that extranuclear or nongenomic actions of these hormones can be mediated by receptors located at the plasma membrane or inside cells, and typically these actions are independent on protein synthesis (Scapin et al, 2010). The rapid actions of thyroid hormones were firstly demonstrated by Segal and Ingbar (1979) showing the T 3 -stimulated glucose transport in rat thymocytes.…”

Maternal-Fetal Thyroid Interactions

“…Interestingly, T4, but not T3, can promote actin polymerization in astrocytes [98] and thus may influence the downregulation of DII activity by a secondary mechanism, perhaps by targeting to lysosomes [9,99]. Moreover, the regulation of actin polymerization and F-actin contents also could contribute to the effects of TH on arborization, axonal transport, and cell-cell contacts during brain development, where the regulation of these factors is fundamental for the organization of guidance molecules such as laminin on the astrocyte plasma membrane and modulates integrin-laminin interactions [3]. T4 was required for integrin clustering and attachment to laminin by integrin in astrocytes [100].…”

“…THs are essential for normal neonatal development in both humans and rodents [3,23,[101][102][103][104] and the experimental work indicated that THs are transported from the mother to the fetus, albeit in limited amounts, and that the fetal brain is exposed to THs before initiation of fetal TH synthesis [1]. In addition, the maternal TH regulates early fetal brain development in human and animal models [2].…”

“…On account of TH action can be controlled in individual cells through selective TH uptake and intracellular TH metabolism, the placenta is an important link in the maternal-fetal communication network for THs which are essential for the normal development and differentiation of the fetus [1][2][3]. Generally, intracellular activation or inactivation of Lthyroxine (T4) and 3,5,3'-triiodothyronine (T3) in turn is determined by three types of iodothyronine deiodinases (Ds), namely DI, DII, and DIII [4][5][6][7].…”