A loss of Cav-1 drives mitochondrial dysfunction and increased glucose uptake in stromal fibroblasts. (A) Western blot analysis shows the targeted stable knock-down of Cav-1 in human stromal fibroblasts, using an siRNA-based approach. Immuno-blotting with β-actin is shown as a control for equal loading. (B) Cav-1 knock-down fibroblasts show a ∼1.8 fold reduction in mitochondrial activity, as measured with the MitoTracker probe, relative to control vector fibroblasts. (C) Cav-1 knock-down fibroblasts show a ∼1.4-fold increase in glucose uptake, using NBD-2-deoxy-glucose, relative to control vector fibroblasts.