2. To form the spindle apparatus and ensure the proper segregation of duplicated chromosomes into daughter cells during cell division (i.e. cytokinesis). The spindle apparatus also regulates the assembly and location of the actin-rich contractile ring that pinches and separates the two daughter cells.
3.To form an internal transport network for the trafficking of vesicles containing essential materials to the rest of the cell. This trafficking is mediated by microtubule associated proteins (MAPs) with motor protein activity such as Kinesin and Dynein.
4. To form a rigid internal core that is used by microtubule-associated motor proteins to generate force and movement in motile structures such as cilia and flagella. A core of microtubules in the neural growth cone and axon also imparts stability and drives neural navigation and guidance.
11]. Changes to these viscoelasticitic properties have been demonstrated in a number of in vitro experiments where physical stresses or the use of agents that selectively disrupt or promote microtubule formation, are applied to cells. In one such case, hypertensive ventricular myocytes were found to be stiffer and more viscous than normotensive ventricular myocytes, a property that was was removed following treatment with colchicine (an inhibitor of microtubule formation) .
It has been well established that myocardial pressure overloading, which results from ventricular hypertrophy, is associated with the loss of cardiac contractility in patients with heart failure . Cooper et al attributed this to an increase in the density of microtubules within cardiac myocytes, where a viscous load is placed on the myofilaments and subsequently impedes sarcomere shortening. In support of their hypothesis, it was shown that treatment with microtubule depolymerizing agents such as colchicine increased contractility .
8]. This remains controversial however, with different studies reporting opposing findings depending on the model used. For example whilst colchicine treatment (and subsequent microtubule depolymerization) was found to promote arrhythmias in a swine model , it had no effect in rabbits .