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- W4229537108 abstract "VOLUME 283 (2008) PAGES 14391–14401 This article has been withdrawn by the authors. The images of 2 and 4 h after NSAID exposure without lansoprazole from Table 1 were reused in Fig. 7 of Pal, C., et al. (2012) J. Biol. Chem. 287, 3495–3509. The image of 0 h after NSAID exposure with lansoprazole was an incorrect image. The NSAID, NSAID + lansoprazole, and Control + lansoprazole images in Fig. 1 were inappropriately presented. The EGF and bFGF panels in Fig. 3A are duplicates. The actin band in lane 2 was reused in lanes 3 and 4 in Figs. 3A and 4A. The first and last lanes of the Bak panel in Fig. 4A are duplicates. The Bax panel in Fig. 4A was spliced. The authors regretfully state that the mistakes occurred while preparing the figures; the authors stand by the overall conclusions of the study. Lansoprazole Protects and Heals Gastric Mucosa from Non-steroidal Anti-inflammatory Drug (NSAID)-induced Gastropathy by Inhibiting Mitochondrial as Well as Fas-mediated Death Pathways with Concurrent Induction of Mucosal Cell RenewalJournal of Biological ChemistryVol. 283Issue 21PreviewWe have investigated the mechanism of antiapoptotic and cell renewal effects of lansoprazole, a proton pump inhibitor, to protect and heal gastric mucosal injury in vivo induced by indomethacin, a non-steroidal anti-inflammatory drug (NSAID). Lansoprazole prevents indomethacin-induced gastric damage by blocking activation of mitochondrial and Fas pathways of apoptosis. Lansoprazole prevents indomethacin-induced up-regulation of proapoptotic Bax and Bak and down-regulation of antiapoptotic Bcl-2 and BclxL to maintain the normal proapoptotic/antiapoptotic ratio and thereby arrests indomethacin-induced mitochondrial translocation of Bax and collapse of mitochondrial membrane potential followed by cytochrome c release and caspase-9 activation. Full-Text PDF Open Access" @default.
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- W4229537108 date "2019-12-01" @default.
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- W4229537108 title "Withdrawal: Lansoprazole protects and heals gastric mucosa from non-steroidal anti-inflammatory drug (NSAID)-induced gastropathy by inhibiting mitochondrial as well as Fas-mediated death pathways with concurrent induction of mucosal cell renewal" @default.
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