Figure 5.
Figure 5. MRP14-/- mice show decreased migration rates of neutrophils during wound healing. (A) Transendothelial migration rates of MRP14+/+ and MRP14-/- granulocytes through a monolayer of bEND5 endothelial cells. Granulocytes were either left untreated or preincubated with arsenite for 30 minutes prior to transendothelial migration to activate p38 MAPK. Bars represent n-fold induction of transmigration rates by arsenite stimulation compared to unstimulated control cells of the appropriate mouse strain. * indicates a statistically significant difference (P ≤ .05). Mean and SD of 5 independent experiments are shown. (B) Mice were wounded as described in “Materials and methods.” The extent of wound closure was determined morphometrically on histologic sections prepared from 5-day old wounds of MRP14-/- mice and MRP+/+ control littermates (8 wounds each). MRP14-/- mice show a significantly accelerated rate of wound closure as compared to MRP14+/+ mice (P ≤ .02). (C-F) Paraffin sections of 5-day-old murine wounds were stained with antibodies directed against cytokeratin 6 (K6, red), cytokeratin 10 (K10, blue), and the granulocyte-specific antigen Ly6G (green), followed by Cy3-, Cy5-, and Cy2-conjugated secondary antibodies, respectively. Panels C and E present sections of MRP14+/+ mice; D and F, sections of MRP14-/- mice at lower (C-D) or higher (E-F) magnifications (bars represent 100 μm). MRP14-/- mice show a significantly lower number of Ly6G+ granulocytes in their granulation tissue. Figures shown are representative for 8 animals from each genotype analyzed.

MRP14-/- mice show decreased migration rates of neutrophils during wound healing. (A) Transendothelial migration rates of MRP14+/+ and MRP14-/- granulocytes through a monolayer of bEND5 endothelial cells. Granulocytes were either left untreated or preincubated with arsenite for 30 minutes prior to transendothelial migration to activate p38 MAPK. Bars represent n-fold induction of transmigration rates by arsenite stimulation compared to unstimulated control cells of the appropriate mouse strain. * indicates a statistically significant difference (P ≤ .05). Mean and SD of 5 independent experiments are shown. (B) Mice were wounded as described in “Materials and methods.” The extent of wound closure was determined morphometrically on histologic sections prepared from 5-day old wounds of MRP14-/- mice and MRP+/+ control littermates (8 wounds each). MRP14-/- mice show a significantly accelerated rate of wound closure as compared to MRP14+/+ mice (P ≤ .02). (C-F) Paraffin sections of 5-day-old murine wounds were stained with antibodies directed against cytokeratin 6 (K6, red), cytokeratin 10 (K10, blue), and the granulocyte-specific antigen Ly6G (green), followed by Cy3-, Cy5-, and Cy2-conjugated secondary antibodies, respectively. Panels C and E present sections of MRP14+/+ mice; D and F, sections of MRP14-/- mice at lower (C-D) or higher (E-F) magnifications (bars represent 100 μm). MRP14-/- mice show a significantly lower number of Ly6G+ granulocytes in their granulation tissue. Figures shown are representative for 8 animals from each genotype analyzed.

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