1991
DOI: 10.1016/0090-6980(91)90020-g
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Calicum channel blockers and prostaglandin generation by gastric surface epithelial cells

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Cited by 4 publications
(4 citation statements)
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“…Rather than the influx across the plasma membrane, the release from the intracellular store was suggested as a mechanism in the case of C10 33. However, this explanation is still controversial because it has also been reported that neither ethanol treatment40,41 nor heat shock42 cause an increase in [Ca 2+ ] i (and even cytotoxicity) in the Ca 2+ ‐free medium, whereas they do cause such an increase in the presence of Ca 2+ . Our future studies will focus on the investigation of the mechanisms by which C12 increases and amino acids decrease [Ca 2+ ] i .…”
Section: Discussionmentioning
confidence: 99%
“…Rather than the influx across the plasma membrane, the release from the intracellular store was suggested as a mechanism in the case of C10 33. However, this explanation is still controversial because it has also been reported that neither ethanol treatment40,41 nor heat shock42 cause an increase in [Ca 2+ ] i (and even cytotoxicity) in the Ca 2+ ‐free medium, whereas they do cause such an increase in the presence of Ca 2+ . Our future studies will focus on the investigation of the mechanisms by which C12 increases and amino acids decrease [Ca 2+ ] i .…”
Section: Discussionmentioning
confidence: 99%
“…As a possible mechanism, the perturbation of intracellular Ca 2+ homeostasis may be involved. An injury caused by oxidative stress was reported to relate to the high level of Ca 2+ in the cytosol in 1980s40–42 and recently it has been reported that the cytoprotection and/or the healing of the gastric mucosa, in which prostaglandins are involved, is ascribed to the action of prostaglandins, not to the increase in the level of Ca 2+ in the cytosol 43–45. Our further studies for clarification of the mechanisms behind the cytoprotective action by amino acids will be focused on its relationship with HSPs and Ca 2+ level in the cytosolic compartment of the colon.…”
Section: Discussionmentioning
confidence: 99%
“…The protective effect of dmPGE2 on gastric mucosal cells from damage caused by various noxious agents such as aspirin, taurocholate, and ethanol has been found in in vitro studies [1-4, 8,9], Fukuda et al [5] have shown that extracellular calcium potentiates damage caused by etha nol to dispersed surface epithelial cells isolated from rat gastric mucosa, and that verapamil, a phenylalkylaminesensitive calcium channel blocker, inhibits ethanol-in duced cell damage. Konda et al [6] have demonstrated that ethanol stimulates the influx of calcium into dis persed chief cells from guinea pig stomach by opening La-1+-sensitive calcium channels, thus damaging the cells.…”
Section: Discussionmentioning
confidence: 99%
“…Since several studies suggest the important role of calcium in cell injury [5,6], we performed experiments in the presence and absence of extracellular calcium.…”
Section: Introductionmentioning
confidence: 99%