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. 2009 Apr 21;122(10):1495–1498. doi: 10.1242/jcs.047894

Fig. 3.

Fig. 3.

LRP1 mediates autocrine HSP90α to promote HK migration. (A) The effect of anti-LRP1 neutralizing antibody on HK migration in response to hypoxia or HSP90α. HKs were subjected to colloidal gold migration assays in the presence of either a control IgG or increasing concentrations of an anti-LRP1 neutralizing antibody under hypoxia. (B) Lysates of HKs infected with lentivirus carrying either a control siRNA (lacZ-siRNA) or two siRNAs against LRP1 (RNAi-1 and RNAi-2) were analyzed by western blot with an anti-LRP1 antibody (inset). Colloidal gold migration assays were used to assess the response of the cells to hypoxia or HSP90α (10 μg/ml). (C) Lysates of HKs expressing vector alone, siRNA-1 or siRNA-1 plus a rescuing LRP1 mutant (mlRLP1) were analyzed by western blot with an anti-LRP1 antibody, which detected the p85 subunit of LRP1 and the p150 mLRP1 mutant (Inset). The HKs were then subjected to colloidal gold migration assays. *Statistically significant (P<0.03-0.05) over serum-free controls, n=3 or 4. (D) Hypoxia drives HSP90α secretion. Secreted HSP90α binds LRP1 and promotes migration of HKs (and probably the surrounding LRP1-positive dermal cells, as well, during wound healing). The mechanism, by which hypoxia causes HKs to secrete intracellular HSP90α, remains to be determined.