Cited by 112Pregnancy and preeclampsia studiesAmino Acid Enzymes and MetabolismReproductive System and Pregnancy

Hypoxia reduces expression and function of system A amino acid transporters in cultured term human trophoblasts

Nelson, D. M., Smith, S. D., Furesz, T. C., Sadovsky, Y., Ganapathy, V., Parvin, C. A., Smith, C. H.·2003·American Journal of Physiology-Cell Physiology

Abstract

We tested the hypothesis that hypoxia diminishes the expression and transport of neutral amino acids by system A in full-term human trophoblasts. Cytotrophoblasts from normal human placentas were cultured in standard conditions of 20% O 2 or in 1% and 3% O 2 for 24 h before assay. Neutral amino acid transport for systems A, ASC, and L was assayed at 24 and 72 h by the cluster-tray technique. Hypoxia during the initial 24 h of culture reduced system A transport by 82% in 1% O 2 and by 37% in 3% O 2 ( P < 0.01) compared with standard conditions. Hypoxia during the latter 24 h of the 72 h in culture reduced system A transport by 55% in 1% O 2 and by 20% in 3% O 2 ( P < 0.05) compared with standard conditions at 72 h. Hypoxia (1% O 2) also reduced total amino acid transport by 40% in the more differentiated syncytiotrophoblasts present at 72 h. Northern analysis of trophoblasts in standard conditions showed that subtypes of human amino acid transporter A (hATA1 and hATA2) were each expressed in cytotrophoblasts and syncytiotrophoblasts. Hypoxia decreased expression of hATA1 and hATA2 in both trophoblast phenotypes. We conclude that hypoxia downregulates system A transporter expression and activity in cultured human trophoblasts.

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Crossref · 10.1152/ajpcell.00253.2002

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  • In human placentas in vitro, exposure to acute episodes of hypoxia reduces expression and/or activity of accumulative System A amino acid transporters but increases activity of System L amino acid transport.

    “In human placentas in vitro, exposure to acute episodes of hypoxia reduces expression and/or activity of accumulative System A amino acid transporters but increases activity of System L amino acid transport (313, 412, 547).”

    From Placental Origins of Chronic Disease (2016) · cites this paper as [412]

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Authors
Nelson, D. M., Smith, S. D., Furesz, T. C., Sadovsky, Y., Ganapathy, V., Parvin, C. A., & Smith, C. H.
Affiliations
  • Department of Obstetrics and Gynecology,
  • St. Louis Children's Hospital (US)
  • Augusta University (US)
  • Washington University in St. Louis (US)
Venue
American Journal of Physiology-Cell Physiology
Published
2003-02-01
Volume
284
Issue
2
Pages
C310-C315
ISSN
  • 0363-6143 (ISSN-L)
  • 1522-1563
OpenAlex
W2331656809
Cited by
112
References
40
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 3 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 8 · 2012: 10
FWCI
11.02
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Cell Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
  • Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
Keywords
hypoxia, system A amino acid transporter, human trophoblast, cytotrophoblast, syncytiotrophoblast, neutral amino acid transport, transporter gene expression, placenta, oxygen deprivation
MeSH terms
Hypoxia, Cells, Cultured, Female, Fetal Hypoxia, Fetal Growth Retardation, Humans, Placenta Diseases, Pregnancy, Trophoblasts, Down-Regulation, Amino Acid Transport System A

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