AJP - Cell Physiology, Vol 259, Issue 2 C232-C240, Copyright © 1990 by American Physiological Society
Stretch-induced prostaglandins and protein turnover in cultured skeletal muscle
H. H. Vandenburgh, S. Hatfaludy, I. Sohar and J. Shansky
Department of Pathology, Brown University, Providence, Rhode Island.
Intermittent repetitive mechanical stimulation of differentiated avian
skeletal muscle cells in vitro for 48 h stimulates skeletal muscle growth
[Am. J. Physiol. 256 (Cell Physiol. 25): C674-C682, 1989]. During the first
2-3 h of stimulation, temporary muscle damage occurs based on increases in
creatine kinase efflux, total protein degradation rates, and several
proteinase activites. With continued mechanical stimulation for several
days in serum-containing medium, the proteinase activities return to
control levels, and total protein degradation rates decrease to levels less
than static controls. Decreased protein degradation thus contributes to
stretch-induced cell growth. The efflux of prostaglandins (PG) E2 and F2
alpha but not 6-keto-PGF1 alpha increase with mechanical stimulation.
During the first 5 h of stimulation, PGE2 and PGF2 alpha efflux rates
increase 101 and 41%, respectively. PGE2 efflux returns to control levels
by 24 h of mechanical stimulation, whereas PGF2 alpha efflux is
continuously elevated (41-116%) for at least 48 h. The long-term
stretch-induced elevation of PGF2 alpha efflux correlates with a 52-98%
long-term increase in total protein synthesis rates. The prostaglandin
synthesis inhibitor indomethacin partially blocks early stretch-induced
cell damage and long-term stretch-induced cell growth. The results indicate
that both of these processes are partially dependent on stretch-induced
increases in prostaglandin synthesis.
