Figure 6
Figure 6. FXIIIa modulates MK spreading and FN assembly on type I collagen. (A) Colocalization during FN fibrillogenesis of FXIII-A (green) and pFN (red) at the membrane level of MKs adherent on type I collagen. Scale bar = 10 μm. (B) MK spreading on type I collagen was modulated by TG activity: analysis of MK CD61+ exhibiting stress fibers in the presence of TG inhibitors such as IAA, MDC, and CYS. Results are reported as a percentage of inhibitor-treated MKs adherent to collagen type I compared with MKs treated with PBS alone, and are the means ± SD of 3 different experiments. (C) Effects of IAA treatment on MK spreading and FITC-labeled FN assembly on type I collagen. Cells were stained with tetramethyl rhodamine isothiocyanate–phalloidin and incubated with 25 μg/mL FITC-FN and immunofluorescent dye as described in “Immunofluorescence and confocal microscopy analysis.” Nuclei were counterstained with Hoechst 33288 (blue). Scale bar = 50 μm. *P < .05

FXIIIa modulates MK spreading and FN assembly on type I collagen. (A) Colocalization during FN fibrillogenesis of FXIII-A (green) and pFN (red) at the membrane level of MKs adherent on type I collagen. Scale bar = 10 μm. (B) MK spreading on type I collagen was modulated by TG activity: analysis of MK CD61+ exhibiting stress fibers in the presence of TG inhibitors such as IAA, MDC, and CYS. Results are reported as a percentage of inhibitor-treated MKs adherent to collagen type I compared with MKs treated with PBS alone, and are the means ± SD of 3 different experiments. (C) Effects of IAA treatment on MK spreading and FITC-labeled FN assembly on type I collagen. Cells were stained with tetramethyl rhodamine isothiocyanate–phalloidin and incubated with 25 μg/mL FITC-FN and immunofluorescent dye as described in “Immunofluorescence and confocal microscopy analysis.” Nuclei were counterstained with Hoechst 33288 (blue). Scale bar = 50 μm. *P < .05

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