Aortic endothelial cell during regeneration. Remodeling of cell junctions, stress fibers, and stress fiber-membrane attachment domains.
We have studied in regenerating endothelium of rat thoracic aortas (a) organization of tight and gap junctions by means of morphometry using freeze-fracture electron microscopy, (b) development of cytoplasmic actin microfilament bundles (stress fibers) by means of morphometry using thin section electron microscopy, and (c) distribution of filipin-sterol complexes in the endothelial plasma membrane using thin section and freeze-fracture electron microscopy. The index of complexity for tight junctions and the index expressing the average width of gap junctions were significantly higher in regenerating endothelium than in normal aortic endothelium. In regenerating endothelium, there was a significant increase of the stress fiber to endothelial volume density ratio as compared to normal. Stress fibers were connected to cytoplasmic microfilament condensations located at the abluminal plasma membrane; the surface density of these condensations was significantly increased in regenerating endothelium as compared to normal. Filipin-cholesterol complexes were few or absent at stress fiber-membrane attachment sites but numerous in the remaining endothelial plasma membrane. This morphologic remodeling of the aortic endothelial cell layer may help to explain changes of endothelial cell function occurring in situations associated with increased cell turnover and motion.
D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology; D004727:Endothelium / Q000166:cytology / Q000502:physiology*; D005372:Filipin / Q000032:analysis; D005455:Fluorescent Antibody Technique; D005614:Freeze Fracturing; D007365:Intercellular Junctions / Q000648:ultrastructure*; D008297:Male; D008854:Microscopy, Electron; D051381:Rats; D011919:Rats, Inbred Strains; D012038:Regeneration; D013261:Sterols / Q000032:analysis
D013261:Sterols; D005372:Filipin