SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress

FEBS Lett. 2005 Jun 20;579(16):3376-80. doi: 10.1016/j.febslet.2005.05.002.

Abstract

Under hypertonic conditions the induction of SLC38A2/SNAT2 leads to the stimulation of transport system A and to the increase in the cell content of amino acids. In hypertonically stressed human fibroblasts transfection with two siRNAs for SNAT2 suppressed the increase in SNAT2 mRNA and the stimulation of system A transport activity. Under the same condition, the expansion of the intracellular amino acid pool was significantly lowered and cell volume recovery markedly delayed. It is concluded that the up-regulation of SNAT2 is essential for the rapid restoration of cell volume after hypertonic stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Transport System A / antagonists & inhibitors*
  • Amino Acid Transport System A / genetics*
  • Amino Acid Transport System A / physiology*
  • Amino Acids / metabolism
  • Cell Size
  • Fibroblasts / drug effects
  • Humans
  • Osmotic Pressure
  • RNA Interference*
  • RNA, Messenger / analysis
  • RNA, Messenger / metabolism
  • RNA, Small Interfering / genetics
  • RNA, Small Interfering / pharmacology
  • Saline Solution, Hypertonic / pharmacology
  • Transfection
  • Up-Regulation

Substances

  • Amino Acid Transport System A
  • Amino Acids
  • RNA, Messenger
  • RNA, Small Interfering
  • SLC38A2 protein, human
  • Saline Solution, Hypertonic