Evidence that the cytoskeleton plays a key role in cell adhesion.
A range of pharmacological agents with defined effects on cell metabolism was used to determine the metabolic requirements of three cell adhesion systems: aggregation of cells from the sponge, Ophlitaspongia tenuis; fibronectin-induced adhesion of fibroblasts to substrata and an in vitro murine thymocyte-macrophage interaction. Cell adhesion in all three systems was found to have similar metabolic requirements, implying that the mechanism of cell adhesion has been conserved through evolution. In fact, based on analysis of F-actin organization in fibroblasts, all of the pharmacological agents that inhibited cell adhesion were found to disrupt the cytoskeleton, suggesting that the cytoskeleton plays a central role in the adhesion process, presumably via redistribution of cell surface molecules. This concept was supported by the finding that the same drugs that inhibited cell adhesion inhibited anti-Ig-induced redistribution of surface Ig on B lymphocytes. The drug inhibition studies also revealed that two drugs, bromophenacyl bromide (BPB) and nordihydroguaiaretic acid (NDGA), that were previously believed to be selective inhibitors of arachidonic acid synthesis and metabolism, are also potent disruptors of the cytoskeleton.
D000098:Acetophenones / Q000494:pharmacology; D000199:Actins / Q000378:metabolism; D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects; D002449:Cell Aggregation / Q000187:drug effects; D003599:Cytoskeleton / Q000187:drug effects / Q000502:physiology*; D005353:Fibronectins / Q000494:pharmacology; D007152:Immunologic Capping / Q000187:drug effects; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000187:drug effects / Q000502:physiology; D008264:Macrophages / Q000187:drug effects / Q000502:physiology; D009637:Masoprocol / Q000494:pharmacology; D051379:Mice; D011161:Porifera; D051381:Rats
D000098:Acetophenones; D000199:Actins; D005353:Fibronectins; D009637:Masoprocol; C006821:4-bromophenacyl bromide