Role of microtubules in the contractile dysfunction of hypertrophied myocardium

Zile, Michael R.; Koide, Masaaki; Sato, Hiroshi; Ishiguro, Yoshiki; Conrad, Chester H.; Buckley, J. Michael; Morgan, James P.; Cooper, George

doi:10.1016/s0735-1097(98)00550-6

Cited by 62 publications

(51 citation statements)

References 14 publications

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“…In this work, we have found that microtubule depolymerization increases neither resting nor peak activated Ca 2ϩ levels in normal or hypertrophied cardiocytes (30), and colchicine increases neither cAMP levels, peak activated Ca 2ϩ levels, nor the rate of rise or fall of intracellular Ca 2ϩ in normal or hypertrophied myocardium (32). Nevertheless, it has been suggested that colchicine increases Ca 2ϩ current density and the intracellular Ca 2ϩ transient in adult cardiocytes (13) via ␣,␤-tubulin heterodimers acting as a functional analog of G proteins to activate adenyl cyclase when the free tubulin concentration is increased by microtubule depolymerization.…”

Section: Is There a Specific Link Between Microtubule Network Densitymentioning

confidence: 64%

Cytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunction

Cooper

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Section: Is There a Specific Link Between Microtubule Network Densitymentioning

confidence: 64%

Cytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunction

Cooper

2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…A computer-controlled servo motor system was used to mechanically test the papillary muscles. Data examining the effect of POH and treatment with colchicine on myocardial contractile function from these same papillary muscles have been previously published (52). The current study examined the effect of POH and treatment with colchicine on myocardial constitutive viscoelastic properties.…”

Section: Methodsmentioning

confidence: 96%

“…RV POH was induced by partially occluding the pulmonary artery with a 2.9-mm inner diameter band using previously described methods (52). Briefly, adult cats weighing 2.6-3.9 kg were first anesthetized with ketamine hydrochloride (15 mg/kg im), meperidine (2.2 mg/kg im), and acepromazine maleate (0.25 mg/kg im), intubated, and then placed on a respirator.…”

Section: Pulmonary Artery Bandingmentioning

confidence: 99%

“…Four weeks after PAB or sham operation, catheterization was performed using previously described methods (52). Cats were anesthetized with ketamine hydrochloride (25 mg/kg im).…”

Section: Hemodynamic Studiesmentioning

confidence: 99%

“…After assessment of hemodynamic status by catheterization, RV papillary muscles were isolated using previously described methods (52). A median sternotomy was performed, the pericardium was bluntly dissected away from the heart, and the cat was heparinized (1,000 units iv).…”

Section: Papillary Muscle Isolationmentioning

confidence: 99%

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Constitutive properties of hypertrophied myocardium: cellular contribution to changes in myocardial stiffness

Harris

Baicu

Conrad

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Recent studies have suggested that pressure overload hypertrophy (POH) alters the viscoelastic properties of individual cardiocytes when studied in isolation. However, whether these changes in cardiocyte properties contribute causally to changes in the material properties of the cardiac muscle as a whole is unknown. Accordingly, a selective, isolated, acute change in cardiocyte constitutive properties was imposed in an in vitro system capable of measuring the resultant effect on the material properties of the composite cardiac muscle. POH caused an increase in both myocardial elastic stiffness, from 20.5 ± 1.3 to 28.4 ± 1.8, and viscous damping, from 15.2 ± 1.1 to 19.8 ± 1.5 s (normal vs. POH, P < 0.05), respectively. Recent studies have shown that cardiocyte constitutive properties could be acutely altered by depolymerizing the microtubules with colchicine. Colchicine caused a significant decrease in the viscous damping in POH muscles (19.8 ± 1.5 s at baseline vs. 14.7 ± 1.3 s after colchicine, P < 0.05). Therefore, myocardial material properties can be altered by selectively changing the constitutive properties of one element within this muscle tissue, the cardiocyte. Changes in the constitutive properties of the cardiocytes themselves contribute to the abnormalities in myocardial stiffness and viscosity that develop during POH.

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Induction of cortical oscillations in spreading cells by depolymerization of microtubules

Pletjushkina

Rajfur

Pomorski

et al. 2001

Cell Motil. Cytoskeleton

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Actomyosin-based cortical contractility is a common feature of eukaryotic cells but the capability to produce rhythmic contractions is found in only a few types such as cardiomyocytes. Mechanisms responsible for the acquisition of this capability remain largely unknown. Rhythmic contractility can be induced in non-muscle cells by microtubule depolymerization. Spreading epithelial cells and fibroblasts in which microtubules were depolymerized with nocodazole or colcemid underwent rhythmic oscillations of the body that lasted for several hours before the cells acquired a stable, flattened shape. By contrast, control cells spread and flattened into discoid shapes in a smooth and regular manner. Quantitative analysis of the oscillations showed that they have a period of about 50 seconds. The kinase inhibitors, HA 1077 and H7, and the more specific rho-kinase inhibitor, Y 27632, caused the oscillations to immediately cease and the cells to become flat. Transient increases in cytoplasmic calcium preceded the contractile phase of the oscillations. Wrinkle formation by cells plated on elastic substrata indicated that the contractility of colcemid-treated cells increased in comparison to controls but was drastically decreased after HA 1077 addition. These data suggest that an intact microtubular system normally prevents pulsations by moderating excessive rho-mediated actin myosin contractility. Possible mechanistic interactions between rho-mediated and calcium activated contractile pathways that could produce morphological oscillations are discussed.

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Role of microtubules in the contractile dysfunction of hypertrophied myocardium

Abstract: Excess microtubule density, therefore, is equally important to both cellular and to myocardial contractile dysfunction caused by chronic, severe pressure-overload cardiac hypertrophy.

Cited by 62 publications

References 14 publications

Cytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunction

Cytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunction

Constitutive properties of hypertrophied myocardium: cellular contribution to changes in myocardial stiffness

Induction of cortical oscillations in spreading cells by depolymerization of microtubules

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