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Chang WC Shyu WJ Shi GY Lin MT Jen CJ Wing LY Tang MJ Wu HL 《Journal of biomedical science》1996,3(1):59-66
Treatment of cultured bovine carotid artery endothelial cells with 0.1 µM human plasmin has been reported to induce a receptor-mediated short burst of arachidonate release, which is a pertussis toxin-sensitive and extracellular calcium-dependent reaction. Plasmin-induced calcium influx in cells was significantly inhibited by pretreatment with pertussis toxin, indicating that the former was coupled with a pertussis toxin-sensitive guanosine 5-triphosphate (GTP)-binding protein. Plasmin significantly induced the formation of lysophosphatidylcholine but not lysophosphatidylethanolamine. A cellular phospholipase A2 with an arachidonyl specificity at the sn-2 position of phosphatidylcholine, which required submicromolar calcium, was identified as a cytosolic phospholipase A2 by immunoblot analysis. By a cell-free enzyme activity assay and immunoblot analysis, plasmin was found to induce a translocation of the cytosolic phospholipase A2 from the cytosol to the membrane. Taken together, the results suggest that plasmin bound to its putative receptor and activated a GTP-binding protein coupled to calcium influx channel, followed by translocation and activation of cytosolic phospholipase A2 in endothelial cells. 相似文献
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Wing LY Chen HM Chuang PC Wu MH Tsai SJ 《The Journal of biological chemistry》2005,280(20):19937-19947
Fibroblast growth factor-9 (FGF9) is a potent mitogen that stimulates normal and cancer cell proliferation though the signaling mechanism is not fully understood. In this study, we aimed to unravel the signaling cascades mediate FGF9 actions in human uterine endometrial stromal cell. Our results demonstrate that the mitogenic effect of FGF9 is transduced via two parallel but additive signaling pathways involving mammalian target of rapamycin (mTOR) and extracellular signal-regulated kinase. Activation of mTOR by FGF9 induces p70 ribosomal S6 kinase (S6K1) phosphorylation, cyclin expression, and cell proliferation, which are independent of phosphatidylinositol 3-kinase and Akt. Coimmunoprecipitation analysis demonstrates that mTOR physically associates with S6K1 upon FGF9 treatment, whereas ablation of mTOR activity using RNA interference or pharmacological inhibitor blocks S6K1 phosphorylation and cell proliferation induced by FGF9. Further study demonstrates that activation of mTOR is regulated by a phospholipase Cgamma-controlled calcium signaling pathway. These studies provide evidence to demonstrate, for the first time, that a novel signaling cascade involving phospholipase Cgamma, calcium, mTOR, and S6K1 is activated by FGF9 in a receptor-specific manner. 相似文献
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The effects of various prostaglandins on ornithine decarboxylase (ODC) activity in mammary gland explants from mid-pregnant mice have been tested. PGE1, E2 and I2 elicit a concentration-dependent stimulation of ODC activity. The minimally effective concentrations are 0.5 ug/ml for PGE1 and E2, and 50 ug/ml for PGF2α and 6-keto-PGF1α. The PGE1 effect had a time course identical to that of prolactin. The prolactin action on ODC activity was attentuated by indomethacin, an inhibitor of prostaglandin biosynthesis. Arachidonic acid stimulation ODC activity and its effect was abolished by indomethacin. The phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, potentiated the PGE1 effect on ODC activity. The results suggest that the prostaglandins may modulate prolactin's action of ODC activity via a cAMP dependent mechanism. 相似文献
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Dr. Ming T. Lin Wen-Chi Su Mei-Ling Cheng Kwang-Shien Cheng Wen-Chang Chang Lih-Yuh C. Wing Chauyin J. Jen Hua-Lin Wu 《Journal of biomedical science》1999,6(4):260-268
The effects of fractionated oxidized low density lipoproteins (oxidized LDL) on the growth of vascular smooth muscle cells (VSMC) and their relationship to the formation of lysophosphatidylcholine (lyso-PC) as well as the activation of protein kinase C (PKC) were studied. VSMC were isolated from porcine aorta by explant culture. LDL was isolated from porcine blood by sequential ultracentrifugation and oxidized LDL was obtained by incubating LDL with 5 µM CuSO4 at 37° C for various lengths of time. Our results showed that LDL oxidized for 12 h and eluted from fast protein liquid chromatography at 43 min inhibited the growth of VSMC, and that LDL oxidized for longer than 48 h and eluted at 48 min stimulated the growth of VSMC. The formation of lyso-PC in the oxidized LDL correlated well with its stimulatory effect, suggesting that lyso-PC is responsible for the mitogenic effect of oxidized LDL. This stimulatory effect of oxidized LDL was inhibited by staurosporine, a PKC inhibitor. Treatment with oxidized LDL increased the activity of membrane PKC, but it decreased that of cytosolic PKC, suggesting the translocation of PKC from cytosol to the membrane in the presence of oxidized LDL. These results suggested that the oxidized LDL-stimulated VSMC growth was mediated by the formation of lyso-PC and the activation of PKC. 相似文献
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