The extent of extra-axonal tissue damage determines the levels of CSPG upregulation and the success of experimental axon regeneration in the CNS.

摘要: The failure of mature central nervous system (CNS) projection neurons to regenerate axons over long distances drastically limits the recovery functions lost after various CNS injuries and diseases. Although a number manipulations that stimulate some degree axon regeneration overcomes inhibitory environment injury have been discovered, extent remains very limited, emphasizing need for improved therapies. Regenerating nerve tissue capable supporting their growth, severe extra-axonal damage remodeling may disrupt such environment. Here, we used traumatic mouse optic as model investigate how affects experimental regeneration. Axon was stimulated by shRNA-mediated knockdown (KD) Pten gene expression in retinal ganglion cells, varied changing duration crush. no were spared using either 1 or 5 seconds crush, found KD-stimulated significantly reduced compared with 1 second more did not cause atrophy, but led higher upregulation growth-inhibiting chondroitin sulfate proteoglycan (CSPG) glial scar also enlarged size, less severely damaged tissue. Thus, success axon-regenerating approaches target neuronal intrinsic mechanisms growth is dependent on preservation appropriate environment, which be co-concurrently repaired methods.