Selective Impairment of Taurine Transport by Cyclosporin A in a Human Placental Cell Line

Ramamoorthy, Sammanda; Leibach, Frederick H.; Mahesh, Virendra B.; Ganapathy, Vadivel

doi:10.1203/00006450-199207000-00024

Cited by 28 publications

(8 citation statements)

References 10 publications

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“…At least five different transport systems for neutral amino acids have been identified in the human syncytiotrophoblast using villous tissue fragments (12), in vitro perfused placenta (13)(14)(15), and cultured trophoblast cells (16) and cell lines (17) as well as in plasma membrane vesicles (Table 1). System A mediates the transport of zwitterionic amino acids with small side chains and has not yet been characterized at the molecular level (6).…”

Section: Placental Amino Acid Transportersmentioning

confidence: 99%

Amino Acid Transporters in the Human Placenta

2001

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The following two reviews deal with the important topic of the physiology of amino acid metabolism in the maternal-placental-fetal unit. Dr. Jansson discusses the biology of amino acid transporters and Dr. Cetin reviews studies of amino acid transport and metabolism in experimental animals and humans. Recent work on the relation between abnormalities of amino acid transport and intrauterine growth retardation underline the importance of this topic and of these timely reviews. Alvin Zipursky Editor-in-ChiefAmino Acid Transporters in the Human Placenta THOMAS JANSSONPerinatal Center, Department of Physiology and Pharmacology, Göteborg University, Sweden Amino acid transport across the human placenta is active, mediated by specific transporters in syncytiotrophoblast plasma membranes. Using functional criteria such as substrate specificity and sodium dependence, approximately 15 transport systems have been identified in the human placenta. Recently, the area of molecular biology of amino acid transporters has evolved rapidly and at least 25 cDNA clones coding for mammalian amino acid transporters or transporter subunits have been identified. The primary objective of this review is to integrate the available functional data on placental amino acid transport systems with recent molecular information on mammalian amino acid transporters. Furthermore, models for the mechanisms for net materno-fetal transfer of amino acids are discussed. Finally, the evidence to suggest that alterations in placental amino acid transport systems may play a crucial role in the regulation of fetal growth are presented briefly. The plasma concentrations of most amino acids are higher in the fetus than in the mother (1), suggesting an active transport of amino acids across the human placenta. There are only two cell layers positioned between the maternal and fetal circulation in the human placenta: the syncytiotrophoblast and the fetal capillary endothelium. The endothelium has been shown to be of the continuous type, closely resembling other continuous nonbrain capillaries (2). This endothelial type allows for relatively unrestricted passage of amino acids through pores within the interendothelial cleft (3) and is therefore unlikely to represent a significant barrier to transport of amino acids. Instead, the transport across the polarized plasma membranes of the syncytiotrophoblast probably represents the limiting step in transplacental amino acid transfer. Consequently, isolated microvillous and basal syncytiotrophoblast membranes studied in vitro are particularly valuable experimental systems in elucidating the cellular mechanisms of amino acid transport across the placenta.Amino acids are transported across plasma membranes mediated by transporter proteins. As a result of pioneer work some 50 years ago, in particular originating from Christensen et al. (4), mammalian amino acid transport systems were identified and characterized according to functional criteria such as substrate specificity and sodium dependence.

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Section: Placental Amino Acid Transportersmentioning

confidence: 99%

Amino Acid Transporters in the Human Placenta

2001

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“…The regulation of placental system L and TAUT is less well established. Placental TAUT activity is regulated by taurine itself (32), calcium (41), PKC (40,59), NO (37,59), and cyclosporin A (57). Increases in intracellular Ca 2ϩ concentrations, PKC, and low extracellular pH (7,51,56) all stimulate system L activity.…”

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Regulation of placental amino acid transporter activity by mammalian target of rapamycin

Roos¹,

Kanai²,

Prasad³

et al. 2009

American Journal of Physiology-Cell Physiology

130

135

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“…Prenatal exposure to such compounds is usually an unwanted consequence of maternal drug therapy, e.g., treatment of epilepsy with anticonvulsants (27), cyclosporin exposure in the case of maternal organ transplant (23), or, more catastrophically, treatment of morning sickness with thalidomide (22). Only a few drugs are considered to be unequivocally safe during pregnancy, which imposes severe limitations on maternal gestational drug therapy (21).…”

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confidence: 99%