Figure 2. Debrin upregulates with atherosclerosis and arterial injury.

A, Human peroneal arteries from surgically amputated legs were separated into segments that demonstrated atherosclerosis (“athero”) and segments with minimal or no atherosclerosis. Serial sections of these segments were immunostained for the indicated protein(s) (or with isotype control IgG), and counterstained with Hoechst 33342 (blue, DNA), or stained with hematoxylin and eosin (H&E). (Elastin autofluorescence is included to facilitate identification of the medial/neointimal boundary.) Letters designate the lumen (L), neointima (N), internal elastic lamina (IEL), and media (M); vWF = von Willebrand factor (in endothelial cells). Samples from a single staining session are shown, and represent 9 independent samples with equivalent results. The athero specimen (right) has pathological neointimal thickening (“subject 1,” Figure II of the online-only Data Supplement). Scale bar = 50 μm. B, Drebrin and SM α-actin immunofluorescence intensities in the arterial media were normalized to corresponding DNA fluorescence intensities; the resulting ratios in each group were divided by cognate ratios obtained for “non-athero” control specimens, to obtain “% of control,” plotted as the means ± SE from 9 specimens of each group. Compared with control: *, p < 0.05. C, Injured and contralateral uninjured (“control”) mouse carotid arteries were sectioned serially and immunostained with anti-Drebrin IgG, isotype control IgG, or anti-SM α-actin IgG, as indicated, and counterstained with Hoechst 33342 (blue, DNA). Samples from a single staining session are shown, and represent 4 independent samples with equivalent results. Scale bar = 100 μm. D, Drebrin and SM α -actin immunofluorescence in the arterial media were normalized to DNA fluorescence; these ratios are plotted (“arbitrary units”) as the means ± SE from 4 independent carotid arteries. Compared with control: *, p < 0.01.