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Am J Physiol Heart Circ Physiol (February 11, 2005). doi:10.1152/ajpheart.01162.2004
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Submitted on November 18, 2004
Accepted on January 24, 2005

Lysophosphatidic acid mediated augmentation of cardiomyocyte lipoprotein lipase involves actin cytoskeleton reorganization

Thomas Pulinilkunnil1, Ding An1, Sanjoy Ghosh1, Dake Qi1, Girish Kewalramani1, Gloria Yuen1, Naureen Virk1, Ashraf Abrahan1, and Brian Rodrigues1*

1 Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada

* To whom correspondence should be addressed. E-mail: rodrigue{at}interchange.ubc.ca.

The lipoprotein lipase (LPL) augmenting property of lysophosphatidylcholine (lysoPC) requires formation of lysophosphatidic acid (LPA) (J Mol Cell Cardiol 37:931-38, 2004). Given that the actin cytoskeleton has been implicated in regulating cardiomyocyte LPL, we examined if LPL secretion following LPA involves actin cytoskeleton reassembly. Incubation of myocytes with LPA (1-100 nM) increased basal and heparin releasable (HR-LPL), an effect that was independent of shifts in LPL mRNA. The influence of LPA on myocyte LPL was reflected at the coronary lumen, with substantial increases of enzyme at this location. Incubation of myocytes with cytochalasin D not only blocked LPA induced augmentation of HR-LPL but also abrogated filamentous actin formation. These effects of LPA were likely receptor mediated. Exposure of myocytes to LPA facilitated significant membrane translocation of RhoA, and its downstream effector Rho kinase I (ROCK 1), and blocking this effect with Y-27632 appreciably reduced basal and HR-LPL activity. Incubation of adipose tissue with LPA also significantly enhanced basal and HR-LPL activity, suggesting that sarcomeric actin likely has a limited role in influencing the LPL secretory function of LPA in the myocyte. Comparable to LPA, hyperglycemia also caused significant membrane translocation of RhoA and ROCK 1 in hearts isolated from diazoxide treated animals, effects that were abrogated using insulin. Overall, our data suggests that comparable to hyperglycemia, LPA induced increases in cardiac LPL occurred via posttranscriptional mechanisms and processes that likely required RhoA activation and actin polymerization. Whether this increase in LPL augments triglyceride deposition in the heart leading to eventual impairment in contractile function is currently unknown.




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