SNAT4 isoform of system A amino acid transporter is expressed in human placenta

Desforges, Michelle; Lacey, H; Glazier, Jocelyn D.; Greenwood, Susan; Mynett, K. J.; Speake, P. F.; Sibley, CP

doi:10.1152/ajpcell.00258.2005

Cited by 99 publications

(87 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…System A and system y + L are expressed at high levels in the placenta in the late stage of gestation. These results tend to be consistent with the previous studies [26,34,35]. Moreover, it has been reported that system A plays a key role in glutamine transport from the maternal side into placental cells [18,33].…”

Section: Discussionsupporting

confidence: 93%

Expression and Role of SNAT3 in the Placenta

et al. 2009

View full text Add to dashboard Cite

The number of characters in the abstract; 1079 characters without spaces 2 The number of characters in the entire manuscripts; 28922 characters without spaces The number of illustrations; 8The number of references; 40 3 AbstractGlutamine is the most versatile amino acid and its plasma concentration is the highest of all amino acid. Many transporters are therefore involved in glutamine uptake or efflux. Glutamine is actively released from the placenta into fetal circulation. In this study, we examined the alteration of transporters that transport glutamine into fetal circulation as gestation progresses. High expression levels of system A and y + L were found in the rat placenta in the late period of pregnancy and the expression levels of these transporters increased as gestation progressed (p<0.05). On the other hand, the expression of SNAT3, the system N transporter, was detected in the early period of pregnancy and its expression level decreased as gestation progressed (p<0.05). SNAT3 was also found to be expressed in isolated human primary cytotrophoblast cells and its expression level was decreased by their differentiation into syncytiotrophoblast cells (p<0.05). Since this regulation is closely related to glutamine synthetase expression, SNAT3 may play a key role in providing glutamine corresponding to glutamine synthetase function in the early period of gestation. This is the first report on the expression of SNAT3 in the placenta in the early stage of pregnancy.

show abstract

Section: Discussionsupporting

confidence: 93%

Expression and Role of SNAT3 in the Placenta

et al. 2009

View full text Add to dashboard Cite

show abstract

“…On the contrary, S-TGCs lining the maternal sinusoids seem to be increased in number in the TFAP2C mutant labyrinth. Deregulated levels of SLC38A4, a neutral amino acid transporter in the placenta, have been associated with abnormal fetal birth weight in humans (Desforges et al, 2006;Li et al, 2012). Fig.…”

Section: Discussionmentioning

confidence: 98%

Tpbpa mediated deletion of Tfap2c leads to deregulation of MAPK, P21, AKT and subsequent placental growth arrest

et al. 2016

View full text Add to dashboard Cite

Loss of TFAP2C in mouse leads to developmental defects in the extra-embryonic compartment with lethality at embryonic day (E)7.5. To investigate the requirement of TFAP2C in later placental development, deletion of TFAP2C was induced throughout extraembryonic ectoderm at E6.5, leading to severe placental abnormalities caused by reduced trophoblast population and resulting in embryonic retardation by E8.5. Deletion of TFAP2C in TPBPA + progenitors at E8.5 results in growth arrest of the junctional zone. TFAP2C regulates its target genes Cdkn1a ( previously p21) and Dusp6, which are involved in repression of MAPK signaling. Loss of TFAP2C reduces activation of ERK1/2 in the placenta. Downregulation of Akt1 and reduced activation of phosphorylated AKT in the mutant placenta are accompanied by impaired glycogen synthesis. Loss of TFAP2C led to upregulation of imprinted gene H19 and downregulation of Slc38a4 and Ascl2. The placental insufficiency post E16.5 causes fetal growth restriction, with 19% lighter mutant pups. Knockdown of TFAP2C in human trophoblast choriocarcinoma JAr cells inhibited MAPK and AKT signaling. Thus, we present a model where TFAP2C in trophoblasts controls proliferation by repressing Cdkn1a and activating the MAPK pathway, further supporting differentiation of glycogen cells by activating the AKT pathway.

show abstract

“…SNAT4 (ATA3, SCL38A3) was identified primarily by sequence similarity. It is expressed primarily in liver and skeletal muscle (Sugawara et al 2000b) and has recently been shown to be present in the syncytiotrophoblast of the placenta (Desforges et al 2005). It is not expressed in trophoblast cell lines such as BeWo (Desforges et al 2005).…”

Section: Introductionmentioning

confidence: 99%

“…It is expressed primarily in liver and skeletal muscle (Sugawara et al 2000b) and has recently been shown to be present in the syncytiotrophoblast of the placenta (Desforges et al 2005). It is not expressed in trophoblast cell lines such as BeWo (Desforges et al 2005). Whether it is primarily involved in transport of substrates for system A is not clear, since it may also transport branched-chain amino acids (Sugawara et al 2000b).…”

Section: Introductionmentioning

confidence: 99%

Expression and adaptive regulation of amino acid transport system A in a placental cell line under amino acid restriction

Jones¹,

Ashworth²,

Page³

et al. 2006

Reproduction

View full text Add to dashboard Cite

Trans-placental transport of amino acids is vital for the developing fetus. Using the BeWo cell line as a placental model, we investigated the effect of restricting amino acid availability on amino acid transport system type A. BeWo cells were cultured either in amino acid-depleted (without non-essential amino acids) or control media for 1, 3, 5 or 6 h. System A function was analysed using a(methyl-amino)isobutyric acid (MeAIB) transcellular transport studies. Transporter (sodium coupled neutral amino acid transporter (SNAT1/2)) expression was analysed at mRNA and protein level by Northern and Western blotting respectively. Localisation was carried out using immunocytochemistry. MeAIB transcellular transport was significantly (P < 0.05) increased by incubation of the cells in amino acid-depleted medium for 1 h, and longer incubation times caused further increases in the rate of transfer. However, the initial response was not accompanied by an increase in SNAT2 mRNA; this occurred only after 3 h and further increased for the rest of the 6-h incubation. Similarly, it took several hours for a significant increase in SNAT2 protein expression. In contrast, relocalisation of existing SNAT2 transporters occurred within 30 min of amino acid restriction and continued throughout the 6-h incubation. When the cells were incubated in medium with even lower amino acid levels (without non-essential plus 0.5 3 essential amino acids), SNAT2 mRNA levels showed further significant (P < 0.0001) up-regulation. However, incubation of cells in depleted medium for 6 h caused a significant (P 5 0.014) decrease in the expression of SNAT1 mRNA. System L type amino acid transporter 2 (LAT2) expression was not changed by amino acid restriction, indicating that the responses seen in the system A transporters were not a general cell response. These data have shown that placental cells adapt in vitro to nutritional stress and have identified the physiological, biochemical and genomic mechanisms involved. Reproduction (2006) 131 951-960

show abstract

SNAT4 isoform of system A amino acid transporter is expressed in human placenta

Cited by 99 publications

References 50 publications

Expression and Role of SNAT3 in the Placenta

Expression and Role of SNAT3 in the Placenta

Tpbpa mediated deletion of Tfap2c leads to deregulation of MAPK, P21, AKT and subsequent placental growth arrest

Expression and adaptive regulation of amino acid transport system A in a placental cell line under amino acid restriction

Contact Info

Product

Resources

About