Cell shrinkage evoked by Ca2+‐free solution in rat alveolar type II cells: Ca2+ regulation of Na+–H+ exchange

Murao, Hiroshi; Shimizu, Akira; Hosoi, Keita; Iwagaki, Akitaka; Min, Kyung‐Jin; Kishima, Genichi; Hanafusa, Toshiaki; Kubota, Takeshi; Kato, Masumi; Yoshida, Hideyo; Nakahari, Takashi

doi:10.1113/expphysiol.2004.028837

Cited by 11 publications

(14 citation statements)

References 31 publications

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“…Similar observations have been reported for rat hepatocytes (Martin-Requero et al, 1997) and rat alveolar cells (Murao et al, 2005). Although neither removal of extracellular Ca 2+ nor a chelation of intra-and extracellular Ca 2+ could abolish the hypertonicity-induced alkalinization, the kinetics and magnitude of this alkalinization were significantly affected by the absence of Ca 2+ (Fig.·4).…”

Section: Removal Of Intracellular Casupporting

confidence: 71%

“…On the other hand, Ca 2+ -dependent activation was reported for other conditions, including mitogenic stimulation (Mitsuhashi and Ives, 1988;Garnovskaya et al, 2003a) and elevation of [Ca 2+ ]i by a calcium ionophore or inhibition of the endoplasmic reticulum Ca 2+ -ATPase (Maly et al, 2002). In human alveolar type II cells a decrease of [Ca 2+ ]i has been shown to elicit cell shrinkage (Murao et al, 2005).…”

Section: Removal Of Intracellular Camentioning

confidence: 99%

“…kinase signalling have also been reported to be involved in the activation of NHE (Grinstein et al, 1992;Moor and Fliegel, 1999), and contradicting results exist concerning the involvement of Ca 2+ ions (Grinstein et al, 1985b;Mitsuhashi and Ives, 1988;Murao et al, 2005). In Ehrlich Ascites tumour cells PKC appears to be involved in the hyperosmotic activation of NHE (Pedersen et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Signalling pathways involved in hypertonicity- and acidification-induced activation of Na+/H+ exchange in trout hepatocytes

Ahmed

Pelster

Krumschnabel

2006

Journal of Experimental Biology

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SUMMARY In trout hepatocytes, hypertonicity and cytosolic acidification are known to stimulate Na+/H+ exchanger (NHE) activity, which contributes to recovery of cell volume and intracellular pH (pHi),respectively. The present study investigated the signalling mechanisms underlying NHE activation under these conditions. Exposing trout hepatocytes to cariporide, a specific inhibitor of NHE-1, decreased baseline pHi,completely blocked the hypertonicity-induced increase of pHi and reduced the hypertonicity-induced proton secretion by 80%. Changing extracellular pH (pHe)above and below normal values, and allowing cells to adjust pHi accordingly,significantly delayed alkalinization during hypertonic exposure, whereas following an acid load an enhanced pHi recovery with increasing pHe was seen. Chelating Ca2+, and thereby preventing the hypertonicity-induced increase in intracellular Ca2+ ([Ca2+]i), significantly diminished hypertonic elevation of pHi, indicating that Ca2+signalling might be involved in NHE activation. A reduction in alkalinization and proton secretion was also observed in the presence of the protein kinase A(PKA) inhibitor H-89 or the calmodulin (CaM) inhibitor calmidazolium. A complete inhibition of hypertonic- and acidification-induced changes of pHi concurrent with an increase in hypertonically induced proton efflux was seen with the protein kinase C (PKC) inhibitor chelerythrine. Recovery of pHi following sodium propionate addition was reduced by more than 60% in the presence of cariporide, was sensitive to PKA inhibition, and tended to be reduced by CaM inhibition. In conclusion, we showed that NHE-1 is the main acid secretion mechanism during hypertonicity and recovery following acid loading. In addition, Ca2+-, PKA- and CaM-dependent pathways are involved in NHE-1 activation for recovery of cell volume and pHi. On the other hand, PKC appeared to have an impact on NHE-independent pathways affecting intracellular acid-base homeostasis.

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Section: Removal Of Intracellular Casupporting

confidence: 71%

Section: Removal Of Intracellular Camentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Signalling pathways involved in hypertonicity- and acidification-induced activation of Na+/H+ exchange in trout hepatocytes

Ahmed

Pelster

Krumschnabel

2006

Journal of Experimental Biology

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“…This cover slip was set in a perfusion chamber mounted on the stage of a differential interference contrast microscope (BX50Wi; Olympus, Tokyo, Japan) connected to a video-enhanced contrast system (AR-GUS-10; Hamamatsu Photonics, Hamamatsu, Japan; see Refs. 6,7,10,11,14,20,21,28). Images were recorded continuously using a video recorder.…”

Section: Methodsmentioning

confidence: 99%

cGMP modulation of ACh-stimulated exocytosis in guinea pig antral mucous cells

Saad¹,

Shimamoto²,

Nakahari³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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In guinea pig antral mucous cells, ACh stimulates the Ca2+-regulated exocytosis, which has a characteristics feature: an initial transient phase followed by a sustained phase. The effects of cGMP on ACh-stimulated exocytosis were studied in guinea pig antral mucous cells using video microscopy. cGMP enhanced the frequency of ACh-stimulated exocytotic events, whereas cGMP alone did not induce any exocytotic events under the ACh-unstimulated condition. cGMP did not stimulate either Ca2+ mobilization or cAMP accumulation. The Ca2+ dose-response studies demonstrated that cGMP shifted the dose-response curve upward with no shift to the lower concentration. This indicates that cGMP increased maximal responsiveness of the Ca2+-regulated exocytosis, but not the Ca2+ sensitivity. Moreover, under a condition of ATP depletion by dinitrophenol (DNP) or anoxia (N2 bubbling), ACh evoked only a sustained phase in exocytotic events with no initial transient phase. However, ACh evoked an initial transient phase followed by a sustained phase with addition of cGMP before ATP depletion, whereas only a sustained phase was evoked in a case of cGMP addition after ATP depletion. Thus cGMP-induced enhancement in ACh-stimulated exocytotic events requires ATP, suggesting that cGMP modulates ATP-dependent priming of Ca2+-regulated exocytosis in antral mucous cells. In conclusion, cGMP increases the number of primed granules via acceleration of the ATP-dependent priming, which enhances the Ca2+-regulated exocytosis stimulated by ACh.

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“…While the activity of pHi regulation mechanisms that accompany cell shrinkage has been reported to be regulated by [Ca 2+ ] i (Murao et al, 2005), other reports suggest, however, that an increase in [Ca 2+ ] i was the consequence of changes in pHi Dascalu et al, 1992;Pedersen et al, 1996).…”

Section: +mentioning

confidence: 78%