Lysophosphatidylcholine induces cytotoxicity/apoptosis and IL-8 production of human endothelial cells: Related mechanisms Lysophosphatidylcholine induces cytotoxicity/apoptosis and IL-8 production of human endothelial cells: Related mechanisms

1. Intracortical microstimulation (ICMS) and surface stimulation studies of primate face motor cortex have shown an extensive representation within face motor cortex devoted to movements of the tongue and face; only a very small representation for jaw-closing movements has ever been demonstrated. These data suggest that face motor cortex plays a critical role in the generation of tongue and facial movements but is less important in the generation of jaw-closing movements. Our aim was to determine whether disruption of primate face motor cortical function would indeed interfere with the generation of tongue movements but would not interfere with the generation of jaw-closing movements. 2. The face motor cortex was reversibly inactivated with the use of cooling in two monkeys that were trained to perform both a tongue-protrusion task and a biting task. Recording of single neuronal activity in the cortex beneath the thermode confirmed the reversible inactivation of the cortex. Each task involved a series of trials in which the monkey was required to produce a preset force level for a 0.5-s force holding period; the monkey received a fruit-juice reward if it successfully completed a task trial. Cooling of the ICMS-defined face motor cortex was achieved bilaterally or, in one experiment, unilaterally by circulating coolant through thermodes placed either on intact dura overlying face motor cortex in both monkeys or directly on the exposed pia in one of the monkeys;thermode temperature was lowered to 3-5 degrees C during cooling. Electromyographic (EMG) recordings were also made from masseter, genioglossus, and digastric muscles. 3. During bilateral cooling of the thermodes on the dura overlying the face motor cortex, there was a significant reduction in the success rates for the performance of the tongue-protrusion task in comparison with control series of trials (i.e., precool and postcool) in which the thermodes were kept at 37 degrees C. Quantitative analyses of force and EMG activity showed that the principal deficit was an inability of each monkey to exert sufficient force with its tongue for a sufficient length of time onto the tongue-protrusion task transducer; this deficit was paralleled by a reduction in the level of genioglossus and digastric EMG activity. At 4 min after commencement of rewarming, task performance had returned to control, precool levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Betel quid (BQ) chewing is an oral habit that increases the risk of oral cancer and oral submucous fibrosis (OSF), a precancerous condition showing epithelial atrophy and tissue fibrosis. Persistent fibroblast contraction may induce the fibrotic contracture of tissue. In this study, we found that areca nut extract (ANE) (200–1200 µg/ml) stimulated buccal mucosa fibroblast (OMF)-populated collagen gel contraction. Arecoline but not arecaidine—two areca alkaloids, slightly induced the OMF contraction. Exogenous addition of carboxylesterase (2U/ml) prevented the arecoline- but not ANE-induced OMF contraction. OMF expressed inositol triphosphate (IP3) receptors. ANE-induced OMF (800 µg/ml) contraction was inhibited by U73122 [phospholipase C (PLC) inhibitor] and 2-aminoethoxydiphenyl borate (IP3 receptor antagonist), respectively. Ethylene glycol tetraacetic acid and verapamil, two calcium mobilization modulators, also suppressed the ANE-induced OMF contraction. ANE induced calcium/calmodulin kinase II and myosin light chain (MLC) phosphorylation in OMF. Moreover, W7 (a Ca ²⁺ /calmodulin inhibitor), HA1077 (Rho kinase inhibitor), ML-7 (MLC kinase inhibitor) and cytochalasin B (actin filament polymerization inhibitor) inhibited the ANE-induced OMF contraction. Although ANE elevated reactive oxygen species (ROS) level in OMF, catalase, superoxide dismutase and N -acetyl- l -cysteine showed no obvious effect on ANE-elicited OMF contraction. These results indicate that BQ chewing may affect the wound healing and fibrotic processes in OSF via inducing OMF contraction by ANE and areca alkaloids. AN components-induced OMF contraction was related to PLC/IP3/Ca ²⁺ /calmodulin and Rho signaling pathway as well as actin filament polymerization, but not solely due to ROS production.