trichostatin-a and Spinal-Cord-Injuries

Epigenetic changes associated with aging have been linked to functional and cognitive deficits in the adult CNS. Histone acetylation is involved in the control of the transcription of plasticity and regeneration-associated genes. The intrinsic axon growth capacity in the CNS is negatively regulated by phosphatase and tensin homolog (Pten). Inhibition of Pten is an effective method to stimulate axon growth following an injury to the optic nerve, corticospinal tract (CST), and rubrospinal tract (RST). Our laboratory has previously demonstrated that the deletion of Pten in aged animals diminishes the regenerative capacity in rubrospinal neurons. We hypothesize that changes in the chromatin structure might contribute to this age-associated decline. Here, we assessed whether Trichostatin A (TSA), a histone deacetylases (HDACs) inhibitor, reverses the decline in regeneration in aged Pten

Topics: Aging; Animals; Axons; GAP-43 Protein; Gene Deletion; Gene Expression; Histone Deacetylase Inhibitors; Histone Deacetylases; Hydroxamic Acids; Mice, Transgenic; Motor Activity; Nerve Regeneration; PTEN Phosphohydrolase; Recovery of Function; Spinal Cord; Spinal Cord Injuries