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© The Rockefeller University Press, 0021-9525/1997//963 $5.00
The Journal of Cell Biology, Volume 139, Number 4, , 1997 963-973

Article

Microtubule Stabilization in Pressure Overload Cardiac Hypertrophy



Hiroshi Sato, Toshio Nagai, Dhandapani Kuppuswamy, Takahiro Narishige, Masaaki Koide, Donald R. Menick, and George Cooper, IV

Cardiology Section of the Department of Medicine and the Department of Physiology, Gazes Cardiac Research Institute, Medical University of South Carolina and the Veterans Administration Medical Center, Charleston, South Carolina 29401

Increased microtubule density, for which microtubule stabilization is one potential mechanism, causes contractile dysfunction in cardiac hypertrophy. After microtubule assembly, {alpha}-tubulin undergoes two, likely sequential, time-dependent posttranslational changes: reversible carboxy-terminal detyrosination (Tyr-tubulin {leftrightarrow} Glu-tubulin) and then irreversible deglutamination (Glu-tubulin -> {Delta}2-tubulin), such that Glu- and {Delta}2-tubulin are markers for long-lived, stable microtubules. Therefore, we generated antibodies for Tyr-, Glu-, and {Delta}2-tubulin and used them for staining of right and left ventricular cardiocytes from control cats and cats with right ventricular hypertrophy. Tyr- tubulin microtubule staining was equal in right and left ventricular cardiocytes of control cats, but Glu-tubulin and {Delta}2-tubulin staining were insignificant, i.e., the microtubules were labile. However, Glu- and {Delta}2-tubulin were conspicuous in microtubules of right ventricular cardiocytes from pressure overloaded cats, i.e., the microtubules were stable. This finding was confirmed in terms of increased microtubule drug and cold stability in the hypertrophied cells. In further studies, we found an increase in a microtubule binding protein, microtubule-associated protein 4, on both mRNA and protein levels in pressure-hypertrophied myocardium. Thus, microtubule stabilization, likely facilitated by binding of a microtubule-associated protein, may be a mechanism for the increased microtubule density characteristic of pressure overload cardiac hypertrophy.

Abbreviations used in this paper: EF-1{alpha}, translation elongation factor-1{alpha}; LV, left ventricle; MAP 4, microtubule-associated protein 4; RV, right ventricle.


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