HCO3 −-dependent transient acidification induced by ionomycin in rat submandibular acinar cells

Yoshida, Hideyo; Shimamoto, Chikao; Ito, Shigenori; Daikoku, Eriko; Nakahari, Takashi

doi:10.1007/s12576-010-0095-x

Cited by 2 publications

(8 citation statements)

References 23 publications

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“…i increase following the reintroduction of Ca 2? in cells stimulated by 5 lM IM (data not shown), as previously reported [5].…”

Section: Membrane Potential Measurementssupporting

confidence: 89%

“…exchange is insensitive to 1 lM Gd 3? and depolarization, and accompanied by membrane depolarization [3][4][5]19]. A previous report demonstrated that an increase in extracellular pH enhances the rate of Ca 2?…”

Section: Discussionmentioning

confidence: 99%

“…(1 lM) inhibited an increase in [Ca 2? ] i stimulated by 1 lM, but not by 5 lM [5]. Thus, IM has two actions depending on its concentration, suggesting that 5 lM IM mediates the Ca 2?…”

Section: Introductionmentioning

confidence: 86%

“…Experiments were approved by the Animal Research Committee of Osaka Medical College, and the animals were cared for according to the guidelines of this committee. The procedures for the cell preparations have already been described in detail [5,16]. The submandibular glands were washed with the control solution to remove blood.…”

Section: Cell Preparation and Fluorescence Measurementsmentioning

confidence: 99%

“…was reintroduced (reintroduction of Ca 2? ) [5,6]. The procedure for ''the reintroduction of Ca 2? ''…”

Section: Activation Of Ca 2? Entrymentioning

confidence: 99%

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Membrane potential modulation of ionomycin-stimulated Ca2+ entry via Ca2+/H+ exchange and SOC in rat submandibular acinar cells

et al. 2010

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Ionomycin (IM) at 5 microM mediates the Ca(2+)/H(+) exchange, while IM at 1 microM activates the store-operated Ca(2+) entry channels (SOCs). In this study, the effects of depolarization on both pathways were examined in rat submandibular acinar cells by increasing extracellular K(+) concentration ([K(+)](o)). IM (5 microM, the Ca(2+)/H(+) exchange) increased the intracellular Ca(2+) concentration ([Ca(2+)](i)) to an extremely high value at 151 mM [K(+)](o). However, with increasing [K(+)](o), the rates of Ca(2+) entry decreased in a linear relationship. The reversal potential (E (rev)) for the Ca(2+)/H(+) exchange was +93 mV, suggesting that IM (5 microM) exchanges 1 Ca(2+) for 1 H(+). Thus, depolarization decreases the Ca(2+) influx via the Ca(2+)/H(+) exchange because of its electrogenicity (1 Ca(2+) for 1 H(+)). On the other hand, IM (1 microM, the SOCs) abolished an increase in [Ca(2+)](i) at 151 mM [K(+)](o). With increasing [K(+)](o), the rate of Ca(2+) entry immediately decreased linearly. The E (rev) for the SOC was +3.7 mV, suggesting that the SOCs are nonselective cation channels and less selective for Ca(2+) over Na(+) (P (Ca)/P (Na) = 8.2). Moreover, an increase in extracellular Ca(2+) concentration (20 mM) enhanced the Ca(2+) entry via the SOCs at 151 mM [K(+)](o), suggesting depolarization does not inhibit the SOCs and decreases the driving force for the Ca(2+) entry. This suggests that membrane potential changes induced by a secretory stimulation finely regulate the [Ca(2+)](i) via the SOCs in rat submandibular acinar cells. In conclusion, IM increases [Ca(2+)](i) via two pathways depending on its concentration, the exchange of 1 Ca(2+) for 1 H(+) at 5 muM and the SOCs at 1 microM.

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“…i increase following the reintroduction of Ca 2? in cells stimulated by 5 lM IM (data not shown), as previously reported [5].…”

Section: Membrane Potential Measurementssupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

“…(1 lM) inhibited an increase in [Ca 2? ] i stimulated by 1 lM, but not by 5 lM [5]. Thus, IM has two actions depending on its concentration, suggesting that 5 lM IM mediates the Ca 2?…”

Section: Introductionmentioning

confidence: 86%

Section: Cell Preparation and Fluorescence Measurementsmentioning

confidence: 99%

“…was reintroduced (reintroduction of Ca 2? ) [5,6]. The procedure for ''the reintroduction of Ca 2? ''…”

Section: Activation Of Ca 2? Entrymentioning

confidence: 99%

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Membrane potential modulation of ionomycin-stimulated Ca2+ entry via Ca2+/H+ exchange and SOC in rat submandibular acinar cells

et al. 2010

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Bafilomycin A1 Molecular Effect on ATPase Activity of Subcellular Fraction of Human Colorectal Cancer and Rat Liver

Bychkova,

Bychkov,

Dordevic

et al. 2024

IJMS

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Bafilomycin A1 inhibits V-type H+ ATPases on the molecular level, which acidifies endo-lysosomes. The main objective of the study was to assess the effect of bafilomycin A1 on Ca2+ content, NAADP-induced Ca2+ release, and ATPase activity in rat hepatocytes and human colon cancer samples. Chlortetracycline (CTC) was used for a quantitative measure of stored calcium in permeabilized rat hepatocytes. ATPase activity was determined by orthophosphate content released after ATP hydrolysis in subcellular post-mitochondrial fraction obtained from rat liver as well as from patients’ samples of colon mucosa and colorectal cancer samples. In rat hepatocytes, bafilomycin A1 decreased stored Ca2+ and prevented the effect of NAADP on stored Ca2+. This effect was dependent on EGTA–Ca2+ buffers in the medium. Bafilomycin A1 significantly increased the activity of Ca2+ ATPases of endoplasmic reticulum (EPR), but not plasma membrane (PM) Ca2+ ATPases in rat liver. Bafilomycin A1 also prevented the effect of NAADP on these pumps. In addition, bafilomycin A1 reduced Na+/K+ ATPase activity and increased basal Mg2+ ATPase activity in the subcellular fraction of rat liver. Concomitant administration of bafilomycin A1 and NAADP enhanced these effects. Bafilomycin A1 increased the activity of the Ca2+ ATPase of EPR in the subcellular fraction of normal human colon mucosa and also in colon cancer tissue samples. In contrast, it decreased Ca2+ ATPase PM activity in samples of normal human colon mucosa and caused no changes in colon cancer. Bafilomycin A1 decreased Na+/K+ ATPase activity and increased basal Mg2+ ATPase activity in normal colon mucosa samples and in human colon cancer samples. It can be concluded that bafilomycin A1 targets NAADP-sensitive acidic Ca2+ stores, effectively modulates ATPase activity, and assumes the link between acidic stores and EPR. Bafilomycin A1 may be useful for cancer therapy.

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HCO3 −-dependent transient acidification induced by ionomycin in rat submandibular acinar cells

Cited by 2 publications

References 23 publications

Membrane potential modulation of ionomycin-stimulated Ca2+ entry via Ca2+/H+ exchange and SOC in rat submandibular acinar cells

Membrane potential modulation of ionomycin-stimulated Ca2+ entry via Ca2+/H+ exchange and SOC in rat submandibular acinar cells

Bafilomycin A1 Molecular Effect on ATPase Activity of Subcellular Fraction of Human Colorectal Cancer and Rat Liver

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