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Background:  We previously reported that lysophosphatidic acid (LPA) promoted cardiomyocyte hypertrophy  in vitro  via one of its G protein-coupled receptor subtypes, LPA 3 . In this study, we examined the role of LPA 3  in cardiac hypertrophy induced by isoproterenol (ISO) and myocardial infarction.   Methods:   In vitro , neonatal rat cardiomyocytes (NRCMs) were subjected to LPA 3  knocked-down, or pretreated with a β-adrenergic receptor (β-AR) antagonist (propranolol) before LPA/ISO treatment. Cardiomyocyte size and hypertrophic gene (ANP, BNP) mRNA levels were determined.  In vivo ,LPA    3    -  /  -and wild-type mice were implanted subcutaneously with an osmotic mini-pump containing ISO or vehicle for 2 weeks; echocardiography was performed to determine the heart weight/body weight ratio, cardiomyocyte cross-sectional area, and level of ANP mRNA expression.LPA    3    -  /  -and wild-type mice were subjected to permanent coronary artery ligation or sham surgery for 4 weeks; cardiac function, including the degree of hypertrophy and infarction size, was determined.   Results:   In vitro , we found that knocked-down LPA 3  in NRCMs did not attenuate ISO-induced hypertrophy, and propranolol was unable to abolish LPA-induced hypertrophy.  In vivo , chronic ISO infusion caused cardiac hypertrophy in wild-type mice, while hypertrophic responses to ISO infusion were not attenuated inLPA    3    -  /  -mice. However, in a myocardial infarction (MI) model,LPA    3    -  /  -mice exhibited reduced cardiac hypertrophy compared to wild-type mice at 4 weeks post-MI, which was associated with reduced cardiac function and increased infarct size.   Conclusions:  Our data show that LPA 3  appears to play a protective role in myocardial hypertrophy post-MI, but does not appear to be involved in the hypertrophy that occurs in response to β-AR stimulation  in vivo  and  in vitro . These results implicate LPA-LPA 3  lipid signaling in cardiac hypertrophy occurring after pathological insults like MI, which presents a new variable in β-AR-independent hypertrophy. Thus, modulation of LPA 3  signaling might represent a new strategy for preventing the stressed myocardium from ischemia injury.

Protective Role for LPA3 in Cardiac Hypertrophy Induced by Myocardial Infarction but Not by Isoproterenol