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Effects of melanocortins on fetal development
Author(s) -
Simamura Eriko,
Shimada Hiroki,
Shoji Hiroki,
Otani Hiroki,
Hatta Toshihisa
Publication year - 2011
Publication title -
congenital anomalies
Language(s) - English
Resource type - Journals
eISSN - 1741-4520
pISSN - 0914-3505
DOI - 10.1111/j.1741-4520.2011.00316.x
Subject(s) - medicine , endocrinology , fetus , adrenocorticotropic hormone , melanocortin , biology , melanocortins , leukemia inhibitory factor receptor , leukemia inhibitory factor , receptor , hormone , pregnancy , cytokine , interleukin 6 , genetics
Melanocortins, adrenocorticotropic hormone (ACTH) and α‐, β‐, and γ‐melanocyte‐stimulating hormone (MSH) are produced in the placenta and secreted into embryos/fetuses. ACTH concentrations are higher in fetal plasma than in maternal plasma and peak at mid‐gestation in rats, whereas ACTH production starts in the anterior lobe of the fetal pituitary at later stages. Melanocortin receptors (MC1‐5R), receptors for ACTH and α‐, β‐ and γ‐MSH, are expressed in various adult organs. The specific function of these receptors has been well examined in the hypothalamic‐pituitary‐adrenocortical (HPA) axis and the HPA axis‐like network in the skin, and anti‐inflammatory effects for white blood cells have also been investigated. MC2R and/or MC5R are also expressed in the testis, lung, kidney, adrenal, liver, pancreas, brain and blood cells at different stages in mouse and rat embryos/fetuses. Melanocortins in embryos and fetuses promote maturation of the HPA axis and also contribute to the development of lung, testis, brain and blood cells. Recently, a unique ACTH function was revealed in fetuses: placental ACTH, which is secreted by the maternal leukemia inhibitory factor (LIF), and induces LIF secretion from fetal nucleated red blood cells. Finally, the maternal LIF‐placental ACTH‐fetal LIF signal relay regulates the LIF level and promotes neurogenesis in fetuses, which suggests that ACTH acts as a signal transducer or effector for fetal development in the maternal‐fetal signal pathway.