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AJP - Cell Physiology, Vol 268, Issue 6 C1512-C1519, Copyright © 1995 by American Physiological Society
ARTICLES |
J. G. Chen, A. B. Strawbridge and S. A. Kempson
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202-5120, USA.
This study has focused on the possible influence of microtubules for the regulation of Na(+)-dependent system A neutral amino acid transport in A10 cells, a cultured cell line derived from rat aortic vascular smooth muscle. When microtubules were disrupted by incubating cells for 5 h in serum-free medium containing colchicine, nocodazole, or vinblastine, there was a twofold increase in system A transport (Vmax change). The dose for the disruption of microtubules by colchicine was similar to the dose required for the stimulation of system A. The time course showed that system A stimulation did not occur until widespread disruption of microtubules was established. The stimulation was specific for system A; there were no changes in glucose transport and Na(+)-dependent transport of phosphate and glutamate. Serum refeeding of quiescent cells from 2 days of serum starvation led to stimulation of system A, glucose, and phosphate transport. However, only system A was activated when colchicine was added to the serum-free medium. Addition of colchicine during serum refeeding had no additive effect for the stimulation of system A. The stimulation by both colchicine and serum was blocked by cycloheximide and actinomycin D. These findings suggest that microtubule disruption may activate system A gene expression.
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