A shed form of LDL receptor–related protein–1 regulates peripheral nerve injury and neuropathic pain in rodents
J. Clin. Invest. Alban Gaultier, et al. 118:161 doi:10.1172/JCI32371 [Go to this article.]

Figure 3
sLRP-α regulates cell signaling in vivo and in vitro. (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.