ABSTRACT
In the present study we demonstrate that the quantitative reduction of meta-vinculin expression parallels histological changes during the course of coronary arteriosclerosis. Immunofluorescence stainings of coronary arteries revealed that vinculin distribution resembled that of other smooth muscle-specific cytoskeletal proteins like alpha-actin, caldesmon or myosin light chain kinase in labeling smooth muscle cells brightly. Although close to arteriosclerotic plaques, the cellularity as measured by the density of nuclei was often not significantly altered. Cells of this location expressed markedly reduced amounts of vinculin, suggesting that they are smooth muscle cells of a synthetic phenotype. To determine the fractional meta-vinculin content in arteriosclerotic lesions, we performed densitometric scanning of immunoblots incubated with anti-vinculin monoclonal antibodies reacting with both meta-vinculin (150 kDa) and vinculin (130 kDa). In parallel, each tissue sample was evaluated histologically for the degree of arteriosclerotic alterations according to the morphometric atheroma score of Stratford et al. (n = 13). In type 1 lesions covering slight intimal thickening, meta-vinculin represented 36% (mean, range 35%-39%) of the total vinculin immunoreactivity. In type 2 lesions consisting of fibrous plaques of up to twice the original artery wall thickness, meta-vinculin accounted for 28% (mean, range 22%-35%) of the total vinculin content. Meta-vinculin was substantially reduced in type 3 lesions (mean 13%, range 8%-18%) which are characterized by extensive atheromatous plaques. Thus, the meta-vinculin/vinculin ratio differed significantly between early, intermediate and advanced phases of coronary arteriosclerotic plaque formation.
Subject(s)
Coronary Artery Disease/pathology , Coronary Vessels/chemistry , Muscle Proteins/analysis , Aged , Arteries/chemistry , Arteries/pathology , Coronary Artery Disease/metabolism , Coronary Vessels/pathology , Fluorescent Antibody Technique , Humans , Immunoblotting , Male , Membrane Proteins/analysis , Middle Aged , Muscle, Smooth, Vascular/chemistry , Vimentin/analysis , Vinculin/analysisABSTRACT
The Transantarctic Mountains (TAM), which separate the West Antarctic rift system from the stable shield of East Antarctica, are the largest mountains developed adjacent to a rift. The cause of uplift of mountains bordering rifts is poorly understood. One notion based on observations of troughs next to many uplifted blocks is that isostatic rebound produces a coeval uplift and subsidence. The results of an over-snow seismic experiment in Antarctica do not show evidence for a trough next to the TAM but indicate the extension of rifted mantle lithosphere under the TAM. Furthermore, stretching preceded the initiation of uplift, which suggests thermal buoyancy as the cause for uplift.
