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. Author manuscript; available in PMC: 2010 Sep 25.
Published in final edited form as: Circ Res. 2009 Aug 27;105(7):676–685. doi: 10.1161/CIRCRESAHA.109.201673

Figure 7. H2O2-induced increase in lung microvessel albumin permeability and pulmonary edema formation requires caveolin-1 phosphorylation.

Figure 7

Cav-1-/- mice were injected intravenously with liposomes containing WT- or Y14F-Cav-1 cDNA. After 48 h, lungs were isolated and perfused with H2O2 (0.5 mmol/L) for 30 min. (A) Western blots show increase in Cav-1 phosphorylation in whole lung homogenates induced by H2O2, the absence of Cav-1 in null mice, and exogenous expression of Myc-tagged WT-Cav-1 and Y14F-Cav-1 in cav-1-/- lungs. Note that H2O2 induced phosphorylation of reconstituted WT-Cav-1 in the isolated mouse lung. (B) Effect of H2O2 on pulmonary microvessel 125I-albumin permeability (PS product) in wild-type (cav-1+/+) and cav-1-/- lungs with or without rescue with WT-Cav-1 or Y14F-Cav-1 mutant cDNA. (C) H2O2 induced and increase in lung wet/dry (W/D) weight ratio in cav-1+/+ lungs but not in cav-1-/- lungs. Rescue of Cav-1 expression with WT-Cav-1 but not Y14F-Cav-1 cDNA restored the lung edema response to H2O2. n = 6/each group. * P < 0.05 compared with control groups (cav-1+/+ mouse without H2O2 treatment); †P < 0.05 compared with cav-1+/+ mouse with H2O2 treatment group.