(A) Sciatic nerve was recovered from mice that were uninjured (sham) and from mice that were subjected to CCI for 24 h. The mice that received CCI were treated with sLRP-α (CCI+sLRP-α) or vehicle (CCI) immediately prior to tightening the sutures. Immunoblot analysis shows P-p38 and PGP9.5, an axonal marker and loading control. (B) Densitometric analysis of the ratio of P-p38 to PGP9.5 in uninjured (day 0) vehicle-treated nerve that was subjected to CCI, sLRP-α–treated nerve subjected to CCI, CCI nerve treated with purified sLRP-α–RAP complex, and CCI nerve that was treated with preincubated but not purified sLRP-α–RAP complex (n = 4/group; *P < 0.01 compared with vehicle-treated CCI animals). (C) Extracts from primary Schwann cells were subjected to SDS-PAGE and immunoblot analysis to detect P-p38 and total p38. The cells were treated with sLRP-α (50 nM) or vehicle for 10 min prior to adding TNF-α (1.0 nM) for 10 min. In some cases, the sLRP-α was preincubated with RAP (200 nM) at 37°C prior to treating Schwann cells. (D) Extracts from Schwann cells in culture were subjected to SDS-PAGE and immunoblot analysis to detect P-p38 and total p38. The cells were first treated with sLRP-α (50 nM) or vehicle for 10 min and then with TNF-α for 10 min. In some cases, cells were washed after treatment with sLRP-α and prior to treatment with TNF-α. The blots shown are representative of 3 independent studies.