Td. Oconnell et al., REGULATION OF MYOSIN ISOZYME EXPRESSION BY VITAMIN-D-3 DEFICIENCY AND1,25-DIHYDROXYVITAMIN-D-3 IN THE RAT-HEART, Endocrinology, 134(2), 1994, pp. 899-905
In this report, we demonstrate a significant inverse correlation betwe
en contractility and serum 1,25-dihydroxyvitamin D-3 [1,25-(OH)(2)D-3]
levels and no correlation between contractility and serum levels of c
alcium, phosphate, or PTH. We also examined myosin isozyme distributio
n in vitamin DB-deficient rats, because myosin isozyme distribution ca
n alter contractility. There was a significant increase in the levels
of the V-1 myosin isozyme in animals raised on a vitamin D-3-deficient
diet that maintained normal serum calcium and phosphate levels. There
was no difference in the relative myosin isozyme distribution in anim
als raised on a hypocalcemia-yielding vitamin D-3-deficient diet us. a
nimals raised on a control diet. As increased contractility has been o
bserved in both groups of vitamin D-3-deficient animals, a shift in my
osin isozyme distribution cannot solely explain the increase in contra
ctility previously observed in the vitamin D-3-deficient rat heart. To
determine whether 1,25-(OH)(2)D-3 directly regulates myosin isozyme l
evels, we analyzed myosin isozyme distribution in primary cultures of
ventricular myocytes. We found that 1,25-(OH)(2)D-3 reduces total myos
in levels, but does not alter myosin isozyme distribution. Thus, we sh
ow that the influence of vitamin D-3 status on myosin isozyme expressi
on in the intact rat involves a complex regulatory system of direct an
d indirect effects.