AJP - Heart and Circulatory Physiology, Vol 253, Issue 1 8-15, Copyright © 1987 by American Physiological Society
Modification of sarcolemmal phosphatidylethanolamine N-methylation during heart hypertrophy
V. Panagia, K. Okumura, K. R. Shah and N. S. Dhalla
To evaluate changes in heart sarcolemmal phosphatidylethanolamine (PE)
N-methylation, left ventricular hypertrophy was induced in rabbits by
banding the abdominal aorta for 4, 8, 14, and 22 wk. The degree of cardiac
hypertrophy did not change over the period of time studied. Three catalytic
sites involved in the sequential methyl transfer reactions were examined by
assaying the incorporation of radiolabeled methyl groups from
S-adenosyl-L-methionine (0.055, 10, and 150 microM) into sarcolemmal PE
molecules under optimal conditions. Total N-methylation activity at all
three sites was significantly increased at 4 wk, unaltered at 8 and 14 wk,
and depressed at 22 wk after banding the aorta. Similar biphasic changes
were seen for the individual methylated lipid products
(monomethylphosphatidylethanolamine, dimethylphosphatidylethanolamine, and
phosphatidylcholine) specifically formed at each catalytic site. At all
three sites, alterations in PE N-methylation at 22 wk were associated with
changes in Vmax values without any change in the apparent affinity for
S-adenosyl-L-methionine. In contrast to sarcolemma, a significant increase
of the PE N-methylation activity at sites I and III was observed in the
sarcoplasmic reticular (microsomal) fraction from 22-wk hypertrophied
hearts; the increase in site II was not significant. On the other hand, no
changes in the N-methylation activity of the mitochondrial fraction were
seen at 22 wk after banding. These findings indicate the occurrence of
biphasic alterations in the sarcolemmal PE N-methylation activity during
the presence of a stable degree of hypertrophy.
