Figure 1.
SHARPINfl/fl Pf4-Cre+ platelets show increased spreading on immobilized fibrinogen. Unstimulated platelets were allowed to attach and spread for 30 minutes on fibrinogen, without (A-D) or with PAR4 agonist peptide (I-K) and then stained with an FITC-conjugated anti-αIIb antibody. Images were acquired on a deconvolution microscope with a ×100 oil objective, and the platelet area and perimeter were calculated using ImagePro software. (A,I) SHARPINfl/fl Pf4-Cre−. (B, J) SHARPINfl/fl Pf4-Cre+. Average area (C,K) and average perimeter. n.s., not significant. (D) of spread platelets (n = 9). (E-F) Effect on platelet spreading of ADP and PI 3-kinase antagonists, apyrase, and wortmannin, respectively (n = 4). *P < .05; **P < .01. (G) Surface rendering of αIIb fluorescence in platelets prepared (as in A-B) using Imaris software. (H) Quantification of average filopodial length per unstimulated αIIb-stained platelet calculated using Imaris rendering (as in G) (n = 5).

SHARPINfl/fl Pf4-Cre+ platelets show increased spreading on immobilized fibrinogen. Unstimulated platelets were allowed to attach and spread for 30 minutes on fibrinogen, without (A-D) or with PAR4 agonist peptide (I-K) and then stained with an FITC-conjugated anti-αIIb antibody. Images were acquired on a deconvolution microscope with a ×100 oil objective, and the platelet area and perimeter were calculated using ImagePro software. (A,I) SHARPINfl/fl Pf4-Cre. (B, J) SHARPINfl/fl Pf4-Cre+. Average area (C,K) and average perimeter. n.s., not significant. (D) of spread platelets (n = 9). (E-F) Effect on platelet spreading of ADP and PI 3-kinase antagonists, apyrase, and wortmannin, respectively (n = 4). *P < .05; **P < .01. (G) Surface rendering of αIIb fluorescence in platelets prepared (as in A-B) using Imaris software. (H) Quantification of average filopodial length per unstimulated αIIb-stained platelet calculated using Imaris rendering (as in G) (n = 5).

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