Sh. Buck et al., Altered kinetics of contraction of mouse atrial myocytes expressing ventricular myosin regulatory light chain, AM J P-HEAR, 45(4), 1999, pp. H1167-H1171
Citations number
30
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
To investigate the role of myosin regulatory light chain isoforms as a dete
rminant of the kinetics of cardiac contraction, unloaded shortening velocit
y was determined by the slack-test method in skinned wild-type murine atria
l cells and transgenic cells expressing ventricular regulatory light chain
(MLC2v). Transgenic mice were generated using a 4.5-kb fragment of the muri
ne a-myosin heavy chain promoter to drive high levels of MLC2v expression i
n the atrium. Velocity of unloaded shortening was determined at 15 degrees
C in maximally activating Ca2+ solution (pCa 4.5) containing (in mmol/l) 7
EGTA, 1 free Mg2+, 4 MgATP, 14.5 creatine phosphate, and 20 imidazole (ioni
c strength 180 mmol/l, pH 7.0). Compared with the wild type (n = 10), the u
nloaded shortening velocity of MLC2v-expressing transgenic murine atrial ce
lls (n = 10) was significantly greater (3.88 +/- 1.19 vs. 2.51 +/- 1.08 mus
cle lengths/s, P < 0.05). These results provide evidence that myosin light
chain 2 regulates cross-bridge cycling rate. The faster rate of cycling in
the presence of MLC2v suggests that the MLC2v isoform may contribute to the
greater power-generating capabilities of the ventricle compared with the a
trium.