Microtubule depolymerization with colchicine and hyperpolymerization with paclitaxel modulated the stiffness of single cardiomyocytes against shear in the longitudinal plane.
Does microtubule modulation alter the mechanical stiffness of single cardiomyocytes?
Microtubules specifically modulate the longitudinal shear stiffness of cardiomyocytes, suggesting a mechanism by which cytoskeletal changes influence diastolic dysfunction in heart disease.
Although microtubules are involved in various pathological conditions of the heart including hypertrophy and congestive heart failure, the mechanical role of microtubules in cardiomyocytes under such conditions is not well understood. In the present study, we measured multiple aspects of the mechanical properties of single cardiomyocytes, including tensile stiffness, transverse (indentation) stiffness, and shear stiffness in both transverse and longitudinal planes using carbon fiber-based systems and compared these parameters under control, microtubule depolymerized (colchicine treated), and microtubule hyperpolymerized (paclitaxel treated) conditions. From all of these measurements, we found that only the stiffness against shear in the longitudinal plane was modulated by the microtubule cytoskeleton. A simulation model of the myocyte in which microtubules serve as compression-resistant elements successfully reproduced the experimental results. In the complex strain field that living myocytes experience in the body, observed changes in shear stiffness may have a significant influence on the diastolic property of the diseased heart.
Nishimura et al. (Thu,) reported a other. Microtubule depolymerization (colchicine) and hyperpolymerization (paclitaxel) vs. Control was evaluated on Mechanical properties of single cardiomyocytes (tensile, transverse, and shear stiffness). Microtubule depolymerization with colchicine and hyperpolymerization with paclitaxel modulated the stiffness of single cardiomyocytes against shear in the longitudinal plane.