{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,3]],"date-time":"2025-10-03T09:22:41Z","timestamp":1759483361513},"reference-count":53,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2005,2,4]],"date-time":"2005-02-04T00:00:00Z","timestamp":1107475200000},"content-version":"vor","delay-in-days":6974,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[1986,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Exposure of quiescent density arrested BALB\/c\u20103T3 cells (clone A31) to platelet\u2010derived growth factor (PDGF;6\u201312 ng\/ml) results in a rapid, reversible, time\u2010and dose\u2010dependent removal of vinculin from adhesion plaques (Herman and Pledger, 1985). Potential cellular mechanisms involved in PDGF\u2010induced removal of vinculin from adhesion plaques were examined. Removal of vinculin from adhesion plaques following exposure of cells to PDGF was temperature dependent, occurred in many fibroblast cell lines, and could be mimicked by 12\u2010tetradecanoyl phorbol\u201013\u2010acetate (TPA; 5\u2010125 nM) or melittin (0.35 \u03bcM). Unlike the effect of PDGF, TPA\u2010or melittin\u2010induced vinculin disruption was not reversible. The removal of vinculin from adhesion plaques was inhibited by trifluoroperazine (TFP; 2.5 \u03bcM). 8\u2010(N,N\u2010diethylamino) octyl\u20103,4,5\u2010trimethoxy benzoate (TMB\u20108; 1.0 \u03bcM), mepacrine (220 \u03bcM), n\u2010\u03b1\u2010p\u2010tosyl\u2010L\u2010lysine chloromethylketone (TLCK; 100 \u03bcM), phenylmethoxysulphonylfluoride (PMSF; 500 \u03bcM), and <jats:italic>e<\/jats:italic>\u2010aminocaproic acid (<jats:italic>e<\/jats:italic>\u2010ACA; 100 \u03bcM); however, amiloride (100 \u03bcM), A23187 (20 \u03bcM), and chloroquine (1 mM) were unable to inhibit this effect. Melittin disruption of vinculin was inhibited by (in order of decreasing effectiveness) mepacrine &gt; TMB\u20108 &gt; TFP &gt; leupeptin &gt; PMSF, whereas A23187 and amiloride had no effect. The return of vinculin to adhesion plaques following PDGF treatment required de novo mRNA transcription and protein synthesis and was associated with PDGF\u2010stimulated synthesis of vinculin.<\/jats:p><jats:p>The observation that both PDGF\u2010 and melittin\u2010induced removal of vinculin from adhesion plaques is inhibited by mepacrine suggests that phospholipase activation may be an early and important step in PDGF\u2010induced disruption of vinculin from adhesion plaques. In addition, TFP, TMB\u20108 and protease inhibitor inhibition of both the PDGF and melittin effects on vinculin distribution, coupled with the finding that TPA can mimic the PDGF or melittin response, suggests that Ca<jats:sup>2+<\/jats:sup>, calmodulin, protein kinase C, and \/or proteolysis may play an important role(s) in the removal of vinculin from adhesion plaques following PDGF addition. The lack of effect of A23187 addition on vinculin distribution suggests that alterations in cellular Ca<jats:sup>2+<\/jats:sup> is necessary but not sufficient for vinculin removal from adhesion plaques.<\/jats:p>","DOI":"10.1002\/jcp.1041260116","type":"journal-article","created":{"date-parts":[[2005,2,26]],"date-time":"2005-02-26T13:03:40Z","timestamp":1109423020000},"page":"115-125","source":"Crossref","is-referenced-by-count":26,"title":["Identification of the cellular mechanisms responsible for platelet\u2010derived growth factor induced alterations in cytoplasmic vinculin distribution"],"prefix":"10.1002","volume":"126","author":[{"given":"B.","family":"Herman","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. A.","family":"Harrington","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"N. 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