| Abstract No.: | A-C1119 |
| Country: | Canada |
| | |
| Title: | THE ROLE OF SOCS IN PERIPHERAL NERVE INJURY |
| | |
| Authors/Affiliations: | 1 Elizabeth I. Girolami*; 1 Michael Haber; 1 Samuel David;
1 Centre for Research in Neuroscience, MUHC and McGill University, Montreal, QC, Canada
|
| | |
| Content: | Wallerian degeneration (WD) in peripheral nerves is initiated by pro-inflammatory cytokines immediately after injury. These pro-inflammatory signals are switched off by various anti-inflammatory mechanisms at the end of the period of WD. The inflammatory response after peripheral nerve injury is thus tightly contained. Although a
great deal of work has focused on the pro-inflammatory mechanisms, little is known of the mechanisms that switch-off the inflammatory response. Suppressors of cytokine signaling (SOCS) proteins, which can inhibit the JAK/STAT pathway appear to be important negative regulators of pro-inflammatory signaling. Our results demonstrate that SOCS1 and SOCS3 have distinct patterns of expression over the course of WD in cut/ligated and crush injuries. Importantly, SOCS1 protein is exclusively expressed by macrophages, and in the cut/ligation injury, which is associated with more extensive inflammation, there are a greater number of SOCS1-positive macrophages. In addition, SOCS1 expression is inversely correlated with both phosphorylation of JAK2 and STAT3 signaling proteins and the expression of pro-inflammatory cytokines IL1β and TNFα. In contrast, SOCS3 expression is restricted to Schwann cells and is negatively correlated with the expression of IL-6, LIF and CNTF. These data suggest that SOCS1 and SOCS3 play different roles in WD and provide a better understanding of some of the regulatory mechanisms that control inflammatory and regenerative processes in the injured peripheral nerve.
|
| | |
| Back |
|
