Coordination of cell shape and motility during retinal microvascular morphogenesis occurs principally through molecular cascades that signal isoactin expression, isoprotein sorting, and cytoskeletal reorganization. Both the assembly state as well as the molecular composition of the isoactin network expressed in vascular cells is tightly regulated. Furthermore, actin cytoskeletal control mechanisms arise through specific protein-protein interactions that sequester isoactin monomers, foster filament cross-linking, or alter polymerization kinetics . Clearly, selective sub-cellular or cell-specific functions are afforded through the specific expression and sorting of multiple actin isoforms encoded by distinct, structurally related genes .
There are multiple lines of genetic, cellular, and biochemical data demonstrating functional diversity of the actin isoforms. Functional distinction is evidenced by altered expression profiles, biophysical properties, cellular localization, and overexpression studies. For example, in retinal pericytes or vascular smooth muscle cells that are actively dividing, nonmuscle isoactins are prevalent; however, when the cells are contractile, a-VSM actin (among other smooth muscle-specific proteins) prevails . Expression of aVSM actin is strongly regulated during wound contraction, as seen in myofibroblasts, during mesangial cell damage in hypertension, and in de-differentiated, intimal vascular smooth muscle cells present in atherosclerotic lesions. This regulated pattern of vascular cell isoactin expression mediates the developmental and disease-related motile- and contractile-mediated events.
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