Document Detail

Effects of melanocortins on fetal development.
MedLine Citation:
PMID:  21595752     Owner:  NLM     Status:  In-Data-Review    
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.
Eriko Simamura; Hiroki Shimada; Hiroki Shoji; Hiroki Otani; Toshihisa Hatta
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Congenital anomalies     Volume:  51     ISSN:  1741-4520     ISO Abbreviation:  Congenit Anom (Kyoto)     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-05-20     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9306292     Medline TA:  Congenit Anom (Kyoto)     Country:  Japan    
Other Details:
Languages:  eng     Pagination:  47-54     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. Congenital Anomalies © 2011 Japanese Teratology Society.
Department of Anatomy I Department of General Education, Life Science (Biology), Kanazawa Medical University, Uchinada, Ishikawa Department of Developmental Biology, Faculty of Medicine, Shimane University, Izumo, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Midkine expression in oral squamous cell carcinoma and leukoplakia.
Next Document:  Hypothyroidism caused by phenobarbital affects patterns of estrous cyclicity in rats.