Xf. Deng et al., Autonomous and growth factor-induced hypertrophy in cultured neonatal mouse cardiac myocytes - Comparison with rat, CIRCUL RES, 87(9), 2000, pp. 781-788
Cultured neonatal rat cardiac myocytes have been used extensively to study
cellular and molecular mechanisms of cardiac hypertrophy. However, there ar
e only a few studies in cultured mouse myocytes despite the increasing use
of genetically engineered mouse models of cardiac hypertrophy. Therefore, w
e characterized hypertrophic responses in low-density, serum-free cultures
of neonatal mouse cardiac myocytes and compared them with rat myocytes. In
mouse myocyte cultures, triiodothyronine (T3), norepinephrine (NE) through
a beta -adrenergic receptor, and leukemia inhibitory factor induced hypertr
ophy by a 20% to 30% increase in [H-3]phenylalanine-labeled protein content
. T3 and NE also increased alpha -myosin heavy chain (MyHC) mRNA and reduce
d beta -MyHC. In contrast, hypertrophic stimuli in rat myocytes, including
alpha (1)-adrenergic agonists, endothelin-1, prostaglandin F-2 alpha interl
eukin 1 beta, and phorbol 12-myristate 13-acetate (PMA), had no effect on m
ouse myocyte protein content. In further contrast with the rat, none of the
se agents increased atrial natriuretic factor or beta -MyHC mRNAs. Acute PM
A signaling was intact by extracellular signal-regulated kinase (ERK1/2) an
d immediate-early gene (fos/jun) activation. Remarkably, mouse but not rat
myocytes had hypertrophy in the absence of added growth factors, with incre
ases in cell area, protein content, and the mRNAs for atrial natriuretic fa
ctor and beta -MyHC. We conclude that mouse myocytes have a unique autonomo
us hypertrophy. On this background, T3, NE, and leukemia inhibitory factor
activate hypertrophy with different mRNA phenotypes, but certain Gq- and pr
otein kinase C-coupled agonists do not.