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Signaling elements involved in amino acid transport responses to altered muscle cell volume
Author(s) -
Low Sylvia Y.,
Rennie Michael J.,
Taylor Peter M.
Publication year - 1997
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.11.13.9367345
Subject(s) - wortmannin , glutamine , phosphatidylinositol , microbiology and biotechnology , biochemistry , protein kinase a , chemistry , kinase , amino acid , biophysics , biology
Skeletal muscle glutamine uptake via the transport system N m is subject to rapid (t 1/2 = ≍1 min) regulation after changes in cell volume by mechanisms that remain to be elucidated. Wortmannin (phosphatidylinositol 3‐kinase inhibitor) but not rapamycin (inhibitor of p70 S6 kinase activation) prevents both hypo‐osmotic swelling‐induced stimulation and hyperosmotic shrinkage‐induced inhibition of Na + ‐dependent glutamine uptake in primary culture of rat skeletal muscle. G‐protein inhibitors (cholera, pertussis toxins) also abolished responses of glutamine transport to cell volume changes whereas these responses were sustained in the presence of G‐protein activators (MAS 7, lysophosphatidic acid). Swelling‐induced activation of glutamine transport does not seem to involve release of autocrine factors because “conditioned” medium from swollen cells has no effect on previously unstimulated cells. System A amino acid transport exhibits responses to cell volume change that are opposite to those of system N m , but these are also blocked by wortmannin. Active phosphatidylinositol 3‐kinase appears to be required to enable muscle cells to exhibit rapid, volume‐induced changes in amino acid transport when suitably stimulated.—Low, S. Y., Rennie, M. J., Taylor, P. M. Signaling elements involved in amino acid transport responses to altered muscle cell volume. FASEB J. 11, 1111–1117 (1997)