Effect of ion composition on the changes in membrane potential induced with several stimuli in rat mast cells

Cabado, Ana G.; Vieytes, Mercedes R.; Botana, Luís M.

doi:10.1002/jcp.1041580213

Cited by 34 publications

(17 citation statements)

References 36 publications

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“…[28][29][30][31][32][33][34] As an increase of cytosolic Ca 2+ could similarly induce apoptotic cell death in nucleated cells, 2 activation of the volume regulated cation channels could similarly participate in the triggering of apoptosis in nucleated cells exposed to an osmotic shock. 3,[9][10][11][12] In summary, we conclude from our results that erythrocyte apoptosis can be induced by different stimuli, such as osmotic shock or oxidative stress, an effect at least partially due to activation of calcium-permeable cation channels.…”

Section: Discussionmentioning

confidence: 99%

Cation channels trigger apoptotic death of erythrocytes

et al. 2003

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Erythrocytes are devoid of mitochondria and nuclei and were considered unable to undergo apoptosis. As shown recently, however, the Ca 2+ -ionophore ionomycin triggers breakdown of phosphatidylserine asymmetry (leading to annexin binding), membrane blebbing and shrinkage of erythrocytes, features typical for apoptosis in nucleated cells. In the present study, the effects of osmotic shrinkage and oxidative stress, well-known triggers of apoptosis in nucleated cells, were studied. Exposure to 850 mOsm for 24 h, to tert-butylhydroperoxide (1 mM) for 15 min, or to glucose-free medium for 48 h, all elicit erythrocyte shrinkage and annexin binding, both sequelae being blunted by removal of extracellular Ca 2+ and mimicked by ionomycin (1 lM). Osmotic shrinkage and oxidative stress activate Ca 2+ -permeable cation channels and increase cytosolic Ca 2+ concentration. The channels are inhibited by amiloride (1 mM), which further blunts annexin binding following osmotic shock, oxidative stress and glucose depletion. In conclusion, osmotic and oxidative stress open Ca 2+ -permeable cation channels in erythrocytes, thus increasing cytosolic Ca 2+ activity and triggering erythrocyte apoptosis.

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Section: Discussionmentioning

confidence: 99%

Cation channels trigger apoptotic death of erythrocytes

et al. 2003

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“…PGE 2 -dependent regulation of cation channels may also play a role in nucleated cells which similarly express cell volume regulatory cation channels. [62][63][64][65][66][67] As increase of cytosolic Ca 2 þ could similarly induce apoptotic cell death in nucleated cells, 1,68 activation of the volume-regulated cation channels might participate in the triggering of apoptosis in nucleated cells exposed to osmotic shock. 8,29,30,69,70 However, it must be pointed out that the mechanisms triggering phosphatidylserine exposure in erythrocytes may be distinct from those inducing apoptosis of nucleated cells.…”

Section: -43mentioning

confidence: 99%

PGE2 in the regulation of programmed erythrocyte death

et al. 2005

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Hyperosmotic shock, energy depletion, or removal of extracellular Cl À activates Ca 2 þ -permeable cation channels in erythrocyte membranes. Subsequent Ca 2 þ entry induces erythrocyte shrinkage and exposure of phosphatidylserine (PS) at the erythrocyte surface. PS-exposing cells are engulfed by macrophages. The present study explored the signalling involved. Hyperosmotic shock and Cl À removal triggered the release of prostaglandin E 2 (PGE 2 ). In whole-cell recording, activation of the cation channels by Cl À removal was abolished by the cyclooxygenase inhibitor diclophenac. In FACS analysis, phospholipase-A 2 inhibitors quinacrine and palmitoyltrifluoromethyl-ketone, and cyclooxygenase inhibitors acetylsalicylic acid and diclophenac, blunted the increase of PS exposure following Cl À removal. PGE 2 (but not thromboxane) induced cation channel activation, increase in cytosolic Ca 2 þ concentration, cell shrinkage, PS exposure, calpain activation, and ankyrin-R degradation. The latter was attenuated by calpain inhibitors-I/II, while PGE 2 -induced PS exposure was not. In conclusion, hyperosmotic shock or Cl À removal stimulates erythrocyte PS exposure through PGE 2 formation and subsequent activation of Ca 2+ -permeable cation channels.

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“…Electrolyte uptake during regulatory cell volume increase is accomplished by activation of Na + channels and/or unselective cation channels [114][115][116][117], of Na + , K + , 2Cl -cotransport [118] and/or of the Na + /H + exchanger [119]. The latter alkalinizes the cell and thus activates the Cl -/HCO Lang/Busch/Völkl cellular electrolyte loss is decreased by inhibition of K + and Cl -channels (table 1).…”

Section: Regulatory Cell Volume Increase (Rvi)mentioning

confidence: 99%

The Diversity of Volume Regulatory Mechanisms

Läng¹,

Busch²,

Völkl³

1998

Cell Physiol Biochem

295

236

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Mammalian cells utilize a wide variety of cell volume regulatory mechanisms. For rapid adjustment of cell volume cells release or accumulate ions through respective channels and transport systems across the cell membrane. The most widely used mechanisms of cell volume regulatory ion release include ion channels and KCl symport. Ion uptake is most frequently mediated by Na⁺ channels, Na⁺, K⁺, 2Cl^– cotransport, and Na⁺/H⁺ exchange. Chronic adjustment of cell osmolarity is accomplished by the formation or accumulation of organic osmolytes, molecules specifically designed to create intracellular osmolarity without interfering with cellular function. The most widely occurring osmolytes are sorbitol, inositol, glycerophosphorylcholine, betaine, taurine, and amino acids. The osmolytes are either synthesized by or transported into shrunken cells. During cell swelling osmolytes can be rapidly degraded or released. Any given cell may utilize several volume-regulatory mechanisms. Moreover, different mechanisms are utilized in different tissues. The diversity of cell volume regulatory mechanisms allows the cells to defend the constancy of cell volume against a myriad of challenges with relatively little impairment of cellular function.

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Effect of ion composition on the changes in membrane potential induced with several stimuli in rat mast cells

Cited by 34 publications

References 36 publications

Cation channels trigger apoptotic death of erythrocytes

Cation channels trigger apoptotic death of erythrocytes

PGE2 in the regulation of programmed erythrocyte death

The Diversity of Volume Regulatory Mechanisms

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