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SNAT2 silencing prevents the osmotic induction of transport system A and hinders cell recovery from hypertonic stress
Author(s) -
Bevilacqua Elena,
Bussolati Ovidio,
Dall‧Asta Valeria,
Gaccioli Francesca,
Sala Roberto,
Gazzola Gian C.,
Franchi-Gazzola Renata
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.05.002
Subject(s) - tonicity , intracellular , stimulation , osmotic shock , chemistry , cell , microbiology and biotechnology , transfection , gene silencing , biophysics , biology , biochemistry , endocrinology , gene
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.

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