Caffeine causes glycerophosphorylcholine accumulation through ryanodine-inhibitable increase of cellular calcium and activation of phospholipase A2 in cultured MDCK cells

Kim, Do Kyung; Jung, Kyu Yong

doi:10.1038/emm.1998.22

Cited by 7 publications

(5 citation statements)

References 21 publications

(47 reference statements)

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“…In the present study, various doses of caffeine (from 1 μM to 10 mM) were used to study the protective mechanisms of caffeine at early phases of COM kidney stone formation, including crystallization, crystal growth, and crystal-cell adhesion28. This range of caffeine dosage was chosen based on the urinary caffeine concentrations measured after 3-h of caffeinated beverage ingestion293031, as well as concentrations used in previous studies on effects of caffeine on the kidney3233. Previous studies have demonstrated that caffeine increased urinary excretion of citric acid34, which is considered as one among several COM crystal growth inhibitors, but on the other hand enhanced urinary calcium excretion9343536.…”

Section: Resultsmentioning

confidence: 99%

Caffeine prevents kidney stone formation by translocation of apical surface annexin A1 crystal-binding protein into cytoplasm: In vitro evidence

Peerapen

Thongboonkerd

2016

Sci Rep

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Recent large 3 cohorts have shown that caffeinated beverage consumption was associated with lower risk of kidney stone disease. However, its protective mechanisms remained unknown and had not been previously investigated. We thus evaluated protective effects of caffeine (1 μM–10 mM) on calcium oxalate monohydrate (COM) kidney stone formation, using crystallization, crystal growth, cell-crystal adhesion, Western blotting, and immunofluorescence assays. The results showed that caffeine reduced crystal number but, on the other hand, increased crystal size, resulting in unchanged crystal mass, consistent with crystal growth that was not affected by caffeine. However, caffeine significantly decreased crystal-binding capacity of MDCK renal tubular cells in a dose-dependent manner. Western blotting and immunofluorescence study of COM crystal-binding proteins revealed significantly decreased level of annexin A1 on apical surface and its translocation into cytoplasm of the caffeine-treated cells, but no significant changes in other COM crystal-binding proteins (annexin A2, α-enolase, HSP70, and HSP90) were observed. Moreover, caffeine decreased intracellular [Ca2+] but increased [Ca2+] secretory index. Taken together, our findings showed an in vitro evidence of the protective mechanism of caffeine against kidney stone formation via translocation of annexin A1 from apical surface into cytoplasm to reduce the crystal-binding capacity of renal tubular epithelial cells.

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Section: Resultsmentioning

confidence: 99%

Caffeine prevents kidney stone formation by translocation of apical surface annexin A1 crystal-binding protein into cytoplasm: In vitro evidence

Peerapen

Thongboonkerd

2016

Sci Rep

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“…In pigmented ciliary epithelial cells [30] and bovine chromaffin cells [31] PLA2-inhibition prevents the activation of the RVDC. In MDCK cells PLA2 is also involved in the synthesis of the organic osmolyte glycerophosphorylcholine (GPC) that is derived from choline via PC and its activation appears to result from a caffeine sensitive, ryanodineinhibitable increase of Ca i [32].…”

Section: Arachidonic Acid and Eicosanoidsmentioning

confidence: 99%

Mechanisms Sensing and Modulating Signals Arising From Cell Swelling

Jakab

Fuerst

Gschwentner

et al. 2002

Cell Physiol Biochem

125

100

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Cell volume alterations are involved in numerous cellular events like epithelial transport, metabolic processes, hormone secretion, cell migration, proliferation and apoptosis. Above all it is a need for every cell to counteract osmotic cell swelling in order to avoid cell damage. The defence against excess cell swelling is accomplished by a reduction of the intracellular osmolarity by release of organic- or inorganic osmolytes from the cell or by synthesis of osmotically less active macromolecules from their specific subunits. De-spite the large amount of experimental data that has accumulated, the intracellular mechanisms underlying the sensing of cell volume perturbations and the activation of volume compensatory processes, commonly summarized as regulatory volume decrease (RVD), are still only partly revealed. Moving into this field opens a complex scenario of molecular rearrangements and interactions involving intracellular messengers such as calcium, phosphoinositides and inositolphosphates as well as phosphoryla-tion/dephosphorylation processes and cytoskeletal reorganization with marked cell type- and tissue specific variations. Even in one and the same cell type significant differences regarding the activated pathways during RVD may be evident. This makes it virtually im-possible to unambigously define common sensing- and sinaling pathways used by differ-ent cells to readjust their celll volume, even if all these pathways converge to the activa-tion of comparatively few sets of effectors serving for osmolyte extrusion, including ion channels and transporters. This review is aimed at providing an insight into the manifold cellular mechanisms and alterations occuring during cell swelling and RVD.

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“…Hence, the caffeine-dependent intracellular signalling pathway in this organism is assumed to be independent of the caspase-dependent apoptotic signalling found in mammalian cells. Furthermore, stimulation with high concentrations of caffeine has been reported to cause a greater than 4-fold increase in AA levels in a mammalian culture cell-line8. Therefore, we measured the survival rate in Hela cells in the presence of the cell-permeable general caspase inhibitor, Q-VD-OPh9 (Fig.…”

Section: Resultsmentioning

confidence: 99%

Arachidonic Acid Enhances Caffeine-Induced Cell Death via Caspase-Independent Cell Death

Kuwayama

2012

Sci Rep

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Caffeine is a globally consumed psychostimulant but can be fatal to cells at overdose exposures. Although caspase-dependent apoptosis plays a role in caffeine-induced cell death, the responsible intracellular signalling cascade remains incompletely understood. The cellular slime mould, Dictyostelium discoideum, does not possess caspase-dependent apoptotic machinery. Here, we observed that ablation of D. discoideum plaA, which encodes a phospholipase A2 (PLA2) homolog, leads to a decreased rate of cell death under high caffeine concentrations and to enhanced cell death with the addition of arachidonic acid. Moreover, the inhibition of PLA2 activity lead to a recovery of the survival rate in caspase-inhibited Hela cervical carcinoma cells under high caffeine concentrations, indicating that caffeine-induced cell death is enhanced via PLA2-dependent signalling. Our results indicate that arachidonic acid may be a general second messenger that negatively regulates caffeine tolerance via a caspase-independent cell death cascade, which leads to multiple effects in eukaryotic cells.

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Caffeine causes glycerophosphorylcholine accumulation through ryanodine-inhibitable increase of cellular calcium and activation of phospholipase A2 in cultured MDCK cells

Cited by 7 publications

References 21 publications

Caffeine prevents kidney stone formation by translocation of apical surface annexin A1 crystal-binding protein into cytoplasm: In vitro evidence

Caffeine prevents kidney stone formation by translocation of apical surface annexin A1 crystal-binding protein into cytoplasm: In vitro evidence

Mechanisms Sensing and Modulating Signals Arising From Cell Swelling

Arachidonic Acid Enhances Caffeine-Induced Cell Death via Caspase-Independent Cell Death

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