Antioxidant activity of sestrin 2 controls neuropathic pain after peripheral nerve injury.

ABSTRACT:

Aims

Neuropathic pain is a chronic debilitating disease that is often unresponsive to currently available treatments. Emerging lines of evidence indicate that reactive oxygen species (ROS) are required for the development and maintenance of neuropathic pain. However, little is known about endogenous mechanisms that neutralize the pain-relevant effects of ROS. In the present study, we tested whether the stress-responsive antioxidant protein Sestrin 2 (Sesn2) blocks the ROS-induced neuropathic pain processing in vivo.

Results

We observed that Sesn2 mRNA and protein expression was up-regulated in peripheral nerves after spared nerve injury, a well-characterized model of neuropathic pain. Sesn2 knockout (Sesn2(-/-)) mice exhibited considerably increased late-phase neuropathic pa

SUBMITTER: Kallenborn-Gerhardt W 

PROVIDER: S-EPMC3869453 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature