The tubulin protein is a major target of drug molecules, and consequently, tubulin inhibitors have attracted great attention as antimitotic antitumor agents for chemotherapeutic use. The effects on tubulin messenger RNA levels and tubulin protein synthesis when treating cells with microtubule-depolymerizing drugs or when directly microinjecting cells with tubulin suggest that non-polymerized tubulin depresses its own synthesis. Accumulation of tubulin protein and an increased array of microtubules have been associated with contractile dysfunction in cardiac myocytes after pressure overload in vivo. Studies have also shown that cardiac activity can increase the amount of beta-tubulin in rat cardiac myocytes. Tubulin production in cultured cardiac myocytes can be regulated directly by mechanical forces. In mechanically challenged hearts, the accumulation of beta-tubulin and the development of contractile dysfunction may be directly related to the mechanical forces imposed on the myocardium during the onset and progression of cardiovascular disease.
Intended for research use only. Not for use in human, therapeutic, or diagnostic applications.