Myosin isoform expression and force generation in cultured
resistance arteries.
Ishibashi, Katsuhiko, and Richard D. Bukoski.
Section of Hypertension and Vascular Research, Departments of
Internal Medicine and Physiology & Biophysics, University of
Texas Medical Branch, Galveston, TX 77555-1065
APStracts 3:0358C, 1996.
Organ culture of mesenteric resistance arteries (MRA) results in a
loss of force generating ability which is prevented by 1,25 (OH)2
vitamin D3 (1,25 vitD). We have tested the hypothesis that the
culture-induced decrease in active stress is associated with altered
myosin isoform expression. Rat MRA were studied immediately (fresh),
or after incubation at 37oC for 48 hr in culture medium (control),
with 300 pg/ml 1,25 vitD (1,25 vitD), or 5 [mu]g/ml insulin
(insulin). Isometric force was measured by myography; myosin heavy
chain (MHC) and regulatory myosin light chain isoform (MLC) content
were determined using SDS-PAGE. Maximal active stress to 100 mM K+
(in mN/mm2) was greater for fresh (147.8 +/-4.9) vs control (109.2+/
-4.6, p=0.001) or insulin (79.6+/-8.6, p<0.001), but not 1,25
vitD (137.4+/-9.5, p=0.197). Organ culture did not alter MLC or MHC
SM-1 isoform content. MHC SM-2 content (nmol/mg prot) was greater in
fresh (0.038+/-0.003) than control (0.026+/- 0.003, p=0.012) and
insulin (0.027+/-0.002, p=0.018); but not 1,25 vitD (0.036+/-0.003,
p=0.693); nonmuscle MHC was observed in insulin. The maximal active
stress response to K+ significantly correlated with SM-2 MHC isoform
content (r2=0.483, p<0.001). We conclude that: 1) arterial
organ culture alters MHC isoform content; 2) SM-2 MHC isoform content
positively correlates with active stress generation; 3) 1,25 vitD
maintains force generation capacity by preventing the shift of MHC
isoform expression; and 4) insulin impairs force generating ability
by lowering MHC SM-2 content and stimulating NMM expression.
Received 9 May 1996; accepted in final form 8 October 1996.
APS Manuscript Number C249-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996