Figure 1
From: Mechanisms of haptoglobin protection against hemoglobin peroxidation triggered endothelial damage
Hb oxidation, endothelial damage, and Hp protection. (a) Endothelial monolayer electrical resistance during treatment with human Hb (huHb, 2 mg/ml), a low/nontoxic level of GOX (2.5 mU/ml), or the combination of huHb+GOX. Only the combination of huHb+GOX resulted in a significant decline of endothelial resistance over time. ECIS traces represent means±S.D. of four replicate measurements. (b) The decline of HPAEC monolayer resistance was morphologically associated with a redistribution of the adherens junction protein β-catenin (red) in fluorescence light microscopy (blue=DAPI-stained nuclei). Imaging of the same specimen region with a correlative SEM revealed intercellular gap formation (arrow head) with intercellular space spanning filopodia in the regions with decreased β-catenin staining. The arrow indicates a conglomerate of Hb aggregates. No changes were observed when cells were only treated with Hb or GOX alone (data not shown). The incubation time in these experiments was 6 h. (c) β-Catenin (red) redistribution in HPAECs was completely prevented when Hp (2 mg/ml) was present during the combined huHb+GOX treatment in confocal laser scanning microscopy images (original magnification × 630)
