Disease relevance of VCL

• In vivo, VCL, ATA, and lamifiban administered 2 minutes after intimal injuries stopped thrombus growth, prevented the cyclic thrombotic process, and induced gradual thrombus dissolution [1].
• Verapamil and semotiadil exhibited a significantly greater effect than diltiazem on the mean ventricular cycle length (VCLmeun), on the maximal ventricular cycle length (VCLmax) and on the standard deviation of the VCL (SD(VCL)) during atrial flutter [2].

High impact information on VCL

• Moreover, there was impaired recruitment of vinculin into focal adhesion complexes of spreading SMCs and disassembly of the smooth muscle alpha-actin-containing cytoskeleton [3].
• Double staining for dystrophin and vinculin showed that the two proteins were not exactly colocalized [4].
• The interaction of actin filaments with two actin-associated proteins, alpha-actinin and vinculin (Mr 130,000 protein), was studied in vitro with viscometry and light and electron microscopy [5].
• A similar disruption in E-cadherin staining was also observed, but colchicine did not affect the distribution of vinculin associated with adherens junctions nor the integrity of the perijunctional actin ring [6].
• The earliest change associated with cell spreading was the accumulation of vinculin and phosphotyrosine in developing focal adhesions, which was followed by stress fiber and microtubule assembly [7].

Chemical compound and disease context of VCL

• Semotiadil has a verapamil type of action on ventricular cycle length during atrial flutter, whereas the disadvantageous prolongation of maximal VCL as well as the dispersion of VCL with semotiadil was only about half those found with verapamil [2].

Biological context of VCL

• Ex vivo, VCL (0.5 to 2 mg/kg) administered as a bolus i.v. injection inhibits risocetin-induced platelet aggregation with a duration of action exceeding 1 h [8].
• The same doses of VCL had no significant effect on platelet count and bleeding time.(ABSTRACT TRUNCATED AT 250 WORDS)[8]
• Calpain mediates progressive plasma membrane permeability and proteolysis of cytoskeleton-associated paxillin, talin, and vinculin during renal cell death [9].
• Molecular cloning and chromosome assignment of porcine vinculin gene (VCL) [10].
• Features studied were actin, microtubules, vinculin, and talin, using immunofluorescence, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and immunoblotting; permeability of the cell sheet; wound healing; and phagocytic capacity [11].

Anatomical context of VCL

• In vivo, the antithrombotic effect of VCL was tested in a model of laser-injured mesentery small arteries and correlated to the ex vivo ristocetin-induced platelet aggregation [8].
• Antithrombotic effect of a recombinant von Willebrand factor, VCL, on nitrogen laser-induced thrombus formation in guinea pig mesenteric arteries [8].
• In cultured rat aortic smooth muscle cells, LPP colocalized with vinculin at focal adhesions but not with p120 catenin or alpha-actinin [12].
• In freshly isolated guinea pig bladder smooth muscle cells, immunofluorescence images showed LPP as linear arrays of punctate, longitudinally oriented staining superimposed with vinculin staining on the plasma membrane surface [12].
• The goal of the present study was to determine the role of calpain in changes in plasma membrane permeability and cytoskeleton-associated paxillin, vinculin, talin, and alpha-actinin levels during acute renal cell death [9].

Associations of VCL with chemical compounds

• The dissimilar calpain inhibitors 3-(4-iodophenyl)-2-mercapto-(Z)-2-propenoic acid (PD150606) or chloroacetic acid N'-[6,7-dichloro-4-phenyl)-3-oxo-3,4-dihydroquinoxalin-2-yl] hydrazide (SJA7029) preserved cytoskeleton-associated paxillin, talin, and vinculin levels and prevented PI influx and LDH release in antimycin A-exposed or hypoxic RPTs [9].
• One important underlying mechanism appears to be regulation of vinculin incorporation into adhesive junctions by cyclic AMP [13].
• In the presence of limiting amounts of liposomes, the alpha-actinin/vinculin ratio was markedly decreased in the liposome fractions [14].
• It is shown in this study that the higher-molecular-mass variant metavinculin and alpha-actinin, also share this property. alpha-Actinin and vinculin were also shown to associate with phosphatidylserine liposomes by chromatography of protein/lipid mixtures on a Bio-Gel A-5m column [14].
• Immunoblotting confirmed significantly greater vinculin in triton-insoluble fractions from monolayer cells compared with follicular cells [13].

Other interactions of VCL

• The relocation of beta-catenin and vinculin away from intercalated discs in failing myocytes may impair the mechanical linkage between N-cadherin and thin filaments and adversely affect myocyte shape [15].
• Since contractile proteins often vary with the cell type and may require different conditions for their interactions, we have developed a procedure which allows the parallel purification of actin-binding protein (ABP), vinculin, alpha-actinin, gelsolin as well as actin and tropomyosin from the same batch of cells [16].
• In conduit intrapulmonary elastic arteries alpha, beta and gamma actin, the 204, 200 and 196 kDa myosin heavy chain (MHC) isoforms and vinculin were localised by immunohistochemistry [17].

Analytical, diagnostic and therapeutic context of VCL

• By immunofluorescence, the 37-kD protein colocalized with actin as well as with vinculin and uvomorulin in oral tissues [18].
• Both PDGF (20 ng/ml) and TPA (100 nM) caused cytosolic alkalinization which occurred after PDGF-induced disruption of vinculin from adhesion plaques, as determined using the pH-sensitive indicator BCECF and Digitized Video Microscopy. PDGF stimulated DNA synthesis and vinculin disruption in a similar dose-dependent fashion [19].
• The complex reorganization of actin microfilament bundles following injury and their relationship to microtubules and vinculin was studied in cells at the wound edge using immunofluorescent scanning laser confocal microscopy and time-lapse videomicroscopy [20].

References