Figure 6
Figure 6. Collagen-induced activation of DDR1 confers resistance to cell death. (A) siRNA-mediated depletion of DDR1 protein shown by immunoblotting (upper panel) increased cell death in collagen-treated L428 Hodgkin lymphoma cells (lower panels). The differences between live populations, defined as Annexin-negative and PI-negative, were significant across 3 experimental replicates (P = .02). (B) Collagen induced the phosphorylation of ectopically expressed DDR1 in DG75 cells. As expected, no phosphorylation of DDR1 was observed following the cultivation of these cells in the absence of collagen. (C) Representative flow cytometry data showed that the addition of collagen to DG75 cells overexpressing DDR1 protected them from etoposide-induced death. The lower panel shows that the differences between live populations, defined as Annexin-negative and PI-negative, were significant across 3 experimental replicates (P = .018).

Collagen-induced activation of DDR1 confers resistance to cell death. (A) siRNA-mediated depletion of DDR1 protein shown by immunoblotting (upper panel) increased cell death in collagen-treated L428 Hodgkin lymphoma cells (lower panels). The differences between live populations, defined as Annexin-negative and PI-negative, were significant across 3 experimental replicates (P = .02). (B) Collagen induced the phosphorylation of ectopically expressed DDR1 in DG75 cells. As expected, no phosphorylation of DDR1 was observed following the cultivation of these cells in the absence of collagen. (C) Representative flow cytometry data showed that the addition of collagen to DG75 cells overexpressing DDR1 protected them from etoposide-induced death. The lower panel shows that the differences between live populations, defined as Annexin-negative and PI-negative, were significant across 3 experimental replicates (P = .018).

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