American Society of Hematology

Figure 4

$Figure 4. Role of Src-family kinases in endothelial permeability induced by P falciparum sonicates in HDMECs. HDMECs in transwells were either untreated or pretreated for 30 minutes at 37°C with the selective Src-family kinase inhibitor PP1 and its inactive analog PP3 (10 μM). (A) PP1 but not PP3 abrogated the changes in FITC-albumin flux induced by parasite sonicates (n = 4). (B) PP1 but not PP3 inhibited the discontinuous staining for ZO-1 and gap formation induced by parasite sonicates. Arrows indicate the presence of interendothelial gaps. (C) PP1 inhibited the redistribution of ZO-1 from the cytoskeleton. Microscopy and Western blot results are representative of 4 experiments. For densitometric analysis of subcellular fractions, each fraction was expressed as a percentage of the total densitometry measurements for all 4 fractions. *P < .05, **P < .01 compared with control values by Student paired t test. (A) Results are expressed as mean (± SD).$

Role of Src-family kinases in endothelial permeability induced by P falciparum sonicates in HDMECs. HDMECs in transwells were either untreated or pretreated for 30 minutes at 37°C with the selective Src-family kinase inhibitor PP1 and its inactive analog PP3 (10 μM). (A) PP1 but not PP3 abrogated the changes in FITC-albumin flux induced by parasite sonicates (n = 4). (B) PP1 but not PP3 inhibited the discontinuous staining for ZO-1 and gap formation induced by parasite sonicates. Arrows indicate the presence of interendothelial gaps. (C) PP1 inhibited the redistribution of ZO-1 from the cytoskeleton. Microscopy and Western blot results are representative of 4 experiments. For densitometric analysis of subcellular fractions, each fraction was expressed as a percentage of the total densitometry measurements for all 4 fractions. *P < .05, **P < .01 compared with control values by Student paired t test. (A) Results are expressed as mean (± SD).

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