Syntaxin-4 and SNAP23 act as exocytic SNAREs to release NGF from cultured Schwann cells.

Nowadays peripheral nerve (PN) injury occurs more frequently, the outcome is often poor because of the ineffective treatment. Once the PN was injured, Schwann cells (SCs) release neurotrophins to guide the regeneration of axons. Recent researches revealed the duration of NGF administration acts a positive role during the nerve regeneration, but the molecular mechanisms of NGF release from SCs are unknown. To investigate components of the exocytic machinery of NGF, we used RT-PCR, Western blot and immunocytochemistry to investigate expressions and locations of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) in rat primary cultured SCs. We found that Syntaxin-4 and SNAP23 were co-localized with NGF by immunocytochemistry. Co-immunoprecipitation (Co-IP) and RNA interference confirmed Syntaxin-4 associated with SNAP23 to regulate the release of NGF from SCs. Knockdown of Syntaxin-4 and SNAP23 dramatically decreased the exocytosis of NGF and inhibited the neurite outgrowth of dorsal root ganglia (DRG). Syntaxin-4 and SNAP23 acted as exocytic SNAREs to release NGF from SCs.

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