Heat shock protein is a key therapeutic target for nerve repair in autoimmune peripheral neuropathy and severe peripheral nerve injury.

Heat shock protein is a key therapeutic target for nerve repair in autoimmune peripheral neuropathy and severe peripheral nerve injury. Brain Behav Immun. 2020 Aug 25;: Authors: Asthana P, Zhang G, Sheikh KA, Him Eddie Ma C Abstract Guillain-Barré syndrome is an autoimmune peripheral neuropathy and a common cause of neuromuscular paralysis. Preceding infection induces the production of anti-ganglioside (GD) antibodies attacking its own peripheral nerves. Damaged axons fail to regrow and to re-innervate target muscles. In severe peripheral nerve injuries (PNI) such as proximal PNIs that requires long-distance axon regeneration, motor functional recovery is virtually non-exist. In mice, regenerating axons must reach target muscle within 35 days (critical period) to reform functional neuromuscular junctions and regain motor function. In current study, forced expression of human heat shock protein (hHsp) 27 completely reversed anti-GD-induced deleterious effects on nerve repair assessed by animal behavioral assays, electrophysiology and histology studies, and the beneficial effect was validated in a second mouse line of hHsp27. Protective effect of hHsp27 on prolonged muscle denervation was examined by performing repeated sciatic nerve crushes to delay regenerating axons from reaching distal muscle from 37 days up to 55 days. Strikingly, hHsp27 was able to extend the critical period of motor functional recovery for up to 55 days, and pr...
Source: Brain, Behavior, and Immunity - Category: Neurology Authors: Tags: Brain Behav Immun Source Type: research