THESIS
2018
x, 41 pages : illustrations (some color) ; 30 cm
Abstract
Permanent disability following spinal cord injury results from the failure of axonal regeneration in central nervous system (CNS). One possible cause is some endogenous suppressors for axon regeneration exist in CNS neurons. Our study established a novel model of gene-silencing screening for axon regeneration. Results showed that the in-vitro screening systematically reflected the role of phosphatases in axon regeneration and we found that TCPTP is an endogenous suppressor of axon regeneration. Further experiments using RNA interference, inhibitor treatment and CRISPR/Cas9 system demonstrated that TCPTP is a potential therapeutic target for both drug treatment and gene therapy. Our mechanism study suggested that the activation of c-Src, but not JAK/STAT pathway is required for TCPTP inh...[
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Permanent disability following spinal cord injury results from the failure of axonal regeneration in central nervous system (CNS). One possible cause is some endogenous suppressors for axon regeneration exist in CNS neurons. Our study established a novel model of gene-silencing screening for axon regeneration. Results showed that the in-vitro screening systematically reflected the role of phosphatases in axon regeneration and we found that TCPTP is an endogenous suppressor of axon regeneration. Further experiments using RNA interference, inhibitor treatment and CRISPR/Cas9 system demonstrated that TCPTP is a potential therapeutic target for both drug treatment and gene therapy. Our mechanism study suggested that the activation of c-Src, but not JAK/STAT pathway is required for TCPTP inhibition induced axon regeneration, although TCPTP inhibition increases neuronal pSTAT3. Our study provides both potential therapeutic target and new mechanism for axon regeneration.
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