THESIS
2014
xi leaves, 31 pages : illustrations (some color) ; 30 cm
Abstract
Loss of intrinsic growth ability of mature CNS neurons is the main reason for the
regeneration failure of CNS axons after injury. Previous studies have identified the
PTEN/mTOR pathway and the JAK/STAT3 pathway as two important machineries
regulating intrinsic regenerative ability. The two pathways worked synergistically to
promote axon regeneration of RGCs after optic nerve injury. In this study, we
co-deleted PTEN and mTOR in corticospinal motor neurons and the results didn’t
reveal further enhance compared with PTEN single deletion. Using delayed PTEN
deletion, our data suggested that intrinsic regenerative ability could be reversed in
mature CSMNs. One-week delayed PTEN deletion promoted robust CST sprouting
which suggested that the developmental decline of growth ability i...[
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Loss of intrinsic growth ability of mature CNS neurons is the main reason for the
regeneration failure of CNS axons after injury. Previous studies have identified the
PTEN/mTOR pathway and the JAK/STAT3 pathway as two important machineries
regulating intrinsic regenerative ability. The two pathways worked synergistically to
promote axon regeneration of RGCs after optic nerve injury. In this study, we
co-deleted PTEN and mTOR in corticospinal motor neurons and the results didn’t
reveal further enhance compared with PTEN single deletion. Using delayed PTEN
deletion, our data suggested that intrinsic regenerative ability could be reversed in
mature CSMNs. One-week delayed PTEN deletion promoted robust CST sprouting
which suggested that the developmental decline of growth ability is reversed in
CSMNs. One-month delayed PTEN deletion after spinal cord injury stimulated CST
axon regeneration beyond the lesion site suggested that injury-induced decrease of
regeneration ability can also be reversed.
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