AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 1 165-R173, Copyright © 1986 by American Physiological Society
Phospholipids, prostaglandin E2, and proteolysis in denervated muscle
J. Turinsky
Soleus muscles of rats were studied up to 16 days after sciatic nerve
transection. At the end of this period the denervated soleus muscles
exhibited decreased content of diphosphatidylglycerol (-44%), normal level
of phosphatidylethanolamine, and increased contents of phosphatidylcholine
(+24%), sphingomyelin (+48%), lysophosphatidylcholine (+110%),
phosphatidylinositol (+37%), and phosphatidylserine (+40%) per milligram of
tissue protein. In studies in vitro, prostaglandin E2 (PGE2) release and
tyrosine release by denervated soleus muscles were 319 and 141%,
respectively, greater than those of sham muscles. An almost complete
inhibition of PGE2 release with 5 X 10(-4) M aspirin or 2.8 X 10(-6) M
indomethacin had no effect on tyrosine release of sham muscles or the
stimulated tyrosine release of the denervated muscles. Addition of 5 X
10(-5) M cycloheximide in the medium resulted in 63% inhibition of PGE2
release by both groups of muscles; concomitant absolute increments in
tyrosine releases by denervated and sham muscles did not statistically
differ. In the presence of both 5 X 10(-5) M cycloheximide and 5 X 10(-4) M
aspirin in the medium, PGE2 production by denervated and sham muscles was
inhibited 87% while tyrosine release of denervated muscles was 108% higher
than that of sham animals. It is concluded that 1) atrophy of denervated
soleus muscle is associated with stimulated activity of tissue
phospholipase A2, increased production of prostaglandin E2, increased total
proteolytic rate, and unchanged rate of protein synthesis; 2) acute
inhibition of PGE2 production does not inhibit the stimulated proteolysis
in denervated muscle; and 3) cycloheximide inhibits PGE2 production by
muscle.
