title: Na+-dependent neutral amino acid transporter ASCT2 is downregulated in seriously traumatized human intestinal epithelial cells.
abstract: OBJECTIVE
  Serious trauma to the body often is associated with changes in protein metabolism in multiple organs and tissues. Clinically, the catabolic response results in a generalized negative nitrogen balance. Nutrition support has been an important component of the care of seriously traumatized patients. However, during states of severe trauma, enterocyte transport function remains unclear. This study aims to quantitate the Na+-dependent neutral amino acid transport and expression of its transporter in traumatically injured Caco-2 cell lines.
  
  
  METHODS
  Transport and transporter of Na+-dependent neutral amino acid in Caco-2 cell lines were characterized. Then the cell lines were cultured under hypoxic, nutrient-deprived, and ischemic conditions for 1, 2, 4, and 6 hours. After severe trauma was performed, we investigated the transport of Na+-dependent neutral amino acids and the expression of transporter protein and mRNA in apical membrane vesicles.
  
  
  RESULTS
  Among the neutral amino acid transporters, only ASCT2 mRNA was amplified successfully. Under nutrient-deprived and ischemic conditions, transport of L-alanine and L-glutamine decreased significantly compared with control (P < 0.01), whereas hypoxia had no significant effect. The changes were associated with a decrease in maximum transport velocity without an influence on transport affinity. Expression of relative transporter proteins and mRNA decreased significantly compared with control (P < 0.01).
  
  
  CONCLUSIONS
  Na+-dependent neutral amino acid transport and its key transporter are differently regulated during state of traumatic injury. It may be of use to provide some strategies targeting the special nutrient requirements and transport capabilities of seriously traumatized patients.
authors.affiliation: Research Institute of General Surgery, Jinling Hospital, Nanjing, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Huang
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.forename: Weiming
authors.initials: W
authors.lastname: Zhu
authors.forename: Qiurong
authors.initials: Q
authors.lastname: Li
authors.forename: Bin
authors.initials: B
authors.lastname: Wang
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D000409:Alanine / Q000378:metabolism; D026962:Amino Acid Transport System ASC / Q000032:analysis / Q000235:genetics*; D000596:Amino Acids / Q000378:metabolism; D015153:Blotting, Western; D018938:Caco-2 Cells; D015687:Cell Hypoxia; D003470:Culture Media; D015536:Down-Regulation; D005973:Glutamine / Q000378:metabolism; D006801:Humans; D007413:Intestinal Mucosa / Q000098:blood supply / Q000378:metabolism*; D007511:Ischemia; D007700:Kinetics; D019344:Lactic Acid / Q000032:analysis; D015778:Minor Histocompatibility Antigens; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018805:Sepsis; D014316:Tritium
chemical_list: D026962:Amino Acid Transport System ASC; D000596:Amino Acids; D003470:Culture Media; D015778:Minor Histocompatibility Antigens; D012333:RNA, Messenger; C420506:SLC1A5 protein, human; D005973:Glutamine; D014316:Tritium; D019344:Lactic Acid; D000409:Alanine