Alpha-tocopherol transfer protein is specifically localized at the implantation site of pregnant mouse uterus.
ABSTRACT Alpha-tocopherol transfer protein (alpha-TTP) was first described to play a major role in maintaining alpha-tocopherol levels in plasma, while alpha-tocopherol was primarily reported to be a factor relevant for reproduction. Expression of alpha-TTP is not only seen in the liver, from where it was first isolated, but also in mouse uterus, depending on its state of pregnancy, stressing the importance of alpha-TTP for embryogenesis and fetal development. The cellular localization of alpha-TTP in mouse uterus is reported here. By immunohistochemistry, alpha-TTP could be localized in the secretory columnar epithelial cells of the pregnant uterus on Days 4.5 and 6.5 postcoitum as well as in the glandular epithelial cells and the inner decidual reaction zone surrounding the implantation site. On Days 8.5 and 10.5 postcoitum (midterm of mouse pregnancy), alpha-TTP could still be detected in the uterine secretory columnar epithelial cells, while in alpha-TTP knockout mice, no immunostaining was visible. It is suggested that alpha-TTP plays a major role in supplying the placenta and consecutively the fetus with alpha-tocopherol throughout pregnancy. We conclude that alpha-tocopherol plays a role in the process of implantation and that alpha-TTP may be necessary for adequate alpha-tocopherol status of the fetus.
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ABSTRACT: α-Tocopherol transfer protein (α-TTP), a 30 kDa cytosolic protein first described to be present in the liver and important for α-tocopherol trafficking, plays a major role in maintaining α-tocopherol levels in plasma, while α-tocopherol is known as the major lipid-soluble antioxidant. Expression of α-TTP has not only been described in animal model liver, but also in diverse other tissues such as rat brain or pregnant mouse uterus, the latter finding stressing the importance of α-TTP for embryogenesis and foetal development. In this study, we report the identification of α-TTP in human liver by anti-human α-TTP monoclonal antibodies made in rat and the cellular localization of α-TTP in term human placenta. By immunohistochemistry, intense staining of α-TTP was seen in syncytiotrophoblast as well as in villous and invading extravillous cytotrophoblast, while basal decidual cells showed slighter, but present staining of α-TTP. Foetal vessel endothelium remained unstained. It is therefore suggested that α-TTP may play a major role in supplying α-tocopherol to the foetus prior to delivery and is likely involved in maintaining adequate α-tocopherol levels in the foetus.Placenta 05/2003; 24(5):439-444. DOI:10.1053/plac.2002.0966 · 3.29 Impact Factor
Article: Vitamin E and transfer proteins.[Show abstract] [Hide abstract]
ABSTRACT: Recently, the intracellular transport as well as cellular uptake and excretion of alpha-tocopherol, the major representative of vitamin E, have been elucidated. Alpha-tocopherol transfer protein has been identified as the major intracellular transport protein for vitamin E, mediating alpha-tocopherol secretion into the plasma via a non-Golgi-dependent pathway, while other binding proteins seem to play a less important role. New information has accumulated concerning the role of this protein in the transport and supply of vitamin E to tissues such as the central nervous system and the feto-maternal unit. The scavenger receptor class B type I receptor, a membrane-bound protein, is capable of transferring vitamin E into the cell, while the ATP-binding cassette transporter A1 can excrete vitamin E out of the cell. Advances in the area of vitamin E metabolism have shown that alpha-CEHC (2,5,7,8-tetramethyl-2-(2'-carboxyethyl)-6-hydroxychroman) and gamma-CEHC (2,7,8-trimethyl-2-(2'-carboxyethyl)-6-hydroxychroman) are formed by a cytochrome p450-mediated process, important for alpha and gamma-tocopherol excretion. Insights into the regulation of vitamin E transport and metabolism on the cellular level have made enormous advances, showing the complex interplay of influx, trafficking, efflux and metabolism of this crucial antioxidant.Current Opinion in Lipidology 07/2003; 14(3):249-54. DOI:10.1097/01.mol.0000073505.41685.09 · 5.80 Impact Factor