Source
Cardiovascular Research Laboratory and Department of Physiology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Abstract
BACKGROUND:
Ventricular remodeling is a consistent feature of the heart's response to hypertrophic stimuli and progression to failure. One cytoskeletal structure in ventricular cardiac myocytes, microtubules, make up only a small proportion of tissue protein but are an essential component for growth in cells. The response of microtubules to different hypertrophic stimuli in postmitotic adult heart has been variable.
METHODS AND RESULTS:
Some models of induced pressure overload hypertrophy have reported microtubule upregulation at the message and protein levels. Furthermore, this microtubule plasticity appears to be responsible for the contractile dysfunction observed in these models. However, studies on other hypertrophic models report little or no microtubule plasticity despite contractile dysfunction. New immunocytochemical, immunoblotting, and mechanical data are reported from a progressive left ventricular pressure overload model, the spontaneously hypertensive rat.
CONCLUSIONS:
No changes were observed in microtubule expression or in either systolic or diastolic function after the reduction or removal of microtubules with colchicine. Thus cellular mechanical dysfunction after hypertrophic stimuli may or may not be mediated microtubule remodeling depending upon the experimental model and conditions.