Hypertrophic scarring and poor intrinsic axon growth capacity constitute major obstacles for spinal cord repair. These processes are tightly regulated by microtubule dynamics. Here, moderate microtubule stabilization decreased scar formation after spinal cord injury in rodents through various cellular mechanisms, including dampening of transforming growth factor-β signaling. It prevented accumulation of chondroitin sulfate proteoglycans and rendered the lesion site permissive for axon regeneration of growth-competent sensory neurons. Microtubule stabilization also promoted growth of central nervous system axons of the Raphe-spinal tract and led to functional improvement. Thus, microtubule stabilization reduces fibrotic scarring and enhances the capacity of axons to grow.

Animals, Axons, Cells, Chondroitin Sulfate Proteoglycans, Cicatrix, Cultured, Female, Ganglia, Kinesin, Microtubules, Paclitaxel, Protein Transport, Rats, Sensory Receptor Cells, Signal Transduction, Smad2 Protein, Spinal, Spinal Cord, Spinal Cord Injuries, Spinal Cord Regeneration, Sprague-Dawley, Transforming Growth Factor beta, animal experiment, animal model, animal tissue, article, cell organelle, chondroitin sulfate, controlled study, functional morphology, hypertrophic scar, injury, microtubule, nerve fiber growth, nerve fiber regeneration, neurology, nonhuman, polysaccharide, priority journal, proteoglycan synthesis, rat, rodent, scar formation, sensory nerve cell, signal transduction, spinal cord injury, stabilization, transforming growth factor beta
dx.doi.org/10.1126/science.1201148, hdl.handle.net/1765/23306
Erasmus MC: University Medical Center Rotterdam

Hellal, F, Hurtado, A, Ruschel, J, Flynn, K.C, Laskowski, C.J, Umlauf, M, … Bradke, F. (2011). Microtubule stabilization reduces scarring and causes axon regeneration after spinal cord injury. Science, 331(6019), 928–931. doi:10.1126/science.1201148