Figure 3
From: Caveolin-3 differentially orchestrates cholinergic and serotonergic constriction of murine airways
Cav-1 expression in cav-3+/+ (WT) and cav-3−/− (KO) mice. (a,b) Tracheal SMC are cav-1-immunoreactive (arrow) in both mouse strains. Bar = 50 µm. (c) Immunoprecipitates (IP) with cav-1 are immunoblotted (IB) for cav-3. Positive Co-IP controls include heart and skeletal muscle from cav-3+/+ mice. Lung input as intact protein lysate from cav-3+/+ mice is blotted and the expression level of cav-3 protein is observed with longer exposure time. The negative control of Co-IP includes beads and antibody in the absence of lysate (no sample). (d) Real-time PCR for cav-1 in cav-3+/+ and cav-3−/− mice trachea and lung homogenates, relative expression is presented as ΔCT compared to β-actin. Lower ΔCT reflects higher expression. Cav-1 was significantly different in tracheal muscle of cav-3−/− and cav-3+/+ mice. (e) Densitometry from cav-1 Western blots, to allow distribution of cav-1 protein compared to β-tubulin to be compared in cav-3+/+ and cav-3−/− mouse trachea and lung. Bars represent SEM. Values are means from separate experiments (n). Each individual experiment was analyzed by the Mann-Whitney U-test. *p ≤ 0.05. (f) Cav-1 staining is strong in tracheal muscle, bronchus and trachea without epithelium and smooth muscle (tracheal rest), while being faint in tracheal epithelium. Tubulin-immunolabelling is observed in the preparations from cav-3+/+ and cav-3−/− mice.
