Fig. 2.

Hypoxia enhanced the destruction of TJs both in vivo and in vitro. A to I C57BL/6 mice were exposed to HH (7600 m above sea level) for 24 h. Brain slices were labelled with immunofluorescence stains for Laminin. Then, they were colabelled for CD31 (A), VE-cadherin (C), occludin (E) or claudin-5 (G), and the fluorescence intensity of CD31 (B), VE-cadherin (D), occludin (F) or claudin-5 (H) in blood vessels was counted separately (*P < 0.05, **P < 0.01 and ***P < 0.001, n = 10). Electron microscope observation of vascular tight junction ultrastructure (I) (E, endothelial cells; L, vascular lumen; TJ, short arrows; endothelial vesicles, long arrows. n = 4). J to M bEnd.3 cells were exposed to 1% O₂ for 24 h or the indicated time. The protein levels of VE-cadherin, occludin, and claudin-5 were determined by Western blot (J) and quantified (K) (* P < 0.05, and *** P < 0.001). The endothelial permeability was detected by TEER (L) and leakage of 40 kD FITC-dextran (M) (*P < 0.05, **P < 0.01 and ***P < 0.001)