Figure 2.
Figure 2. Platelets from mice with DSS-induced colitis have reduced HYAL2 and hyaluronidase activity. Platelets were isolated from untreated control and DSS-treated mice after 7 days. (A) Platelet lysates corresponding to 10 μg of protein were probed for HYAL2 and actin. (B) Densitometry quantification shows that HYAL2 levels are reduced an average of 44% (*P < .05) in platelets from DSS-treated mice compared with control mice. (C) Platelet lysates were compared for their HA-degrading activities by incubation with 60 nM Förster resonance energy transfer–based HA nanoprobes at pH 4.5. Maximum activity was achieved by recombinant hyaluronidase. Platelets from DSS-treated mice exhibit a 60% reduction (*P < .05) in HA-degrading activity compared with platelets from untreated mice. (D) Changes in circulating platelet count before and after DSS-induced colitis (**P < .01). (E) Serum isolated from DSS-treated mice and control mice at 7 days was tested for HA levels (*P < .05).

Platelets from mice with DSS-induced colitis have reduced HYAL2 and hyaluronidase activity. Platelets were isolated from untreated control and DSS-treated mice after 7 days. (A) Platelet lysates corresponding to 10 μg of protein were probed for HYAL2 and actin. (B) Densitometry quantification shows that HYAL2 levels are reduced an average of 44% (*P < .05) in platelets from DSS-treated mice compared with control mice. (C) Platelet lysates were compared for their HA-degrading activities by incubation with 60 nM Förster resonance energy transfer–based HA nanoprobes at pH 4.5. Maximum activity was achieved by recombinant hyaluronidase. Platelets from DSS-treated mice exhibit a 60% reduction (*P < .05) in HA-degrading activity compared with platelets from untreated mice. (D) Changes in circulating platelet count before and after DSS-induced colitis (**P < .01). (E) Serum isolated from DSS-treated mice and control mice at 7 days was tested for HA levels (*P < .05).

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