The role of bicarbonate in regulatory volume decrease (RVD) in the epithelial-derived human breast cancer cell line ZR-75-1

Nicholl, Amanda; Killey, Jennifer; Leonard, M.N.; Garner, Craig C.

doi:10.1007/s00424-001-0771-z

Cited by 13 publications

(7 citation statements)

References 25 publications

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“…Thus, activation of the volume‐sensitive chloride channels by shrinkage could be responsible for the increased chloride conductance of the shrunken cells. The sensitivity of RVI to the potent blockers of sodium and chloride fluxes is in accordance with the findings reported in human breast cancer cells and in the intestinal epithelium (Lionetto et al, 2001; Nicholl et al, 2002). It must be noted that it is not always possible to distinguish whether the effect on RVI is of primary or secondary nature due to observed effects on the isotonic volume at high drug concentrations.…”

Section: Discussionsupporting

confidence: 89%

Regulatory and necrotic volume increase in boar spermatozoa

Petrunkina

Jebe

Töpfer‐Petersen

2005

Journal Cellular Physiology

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Spermatozoa of many species initially respond to hypotonicity as perfect osmometers. Thereafter they undergo a regulatory process resulting in a decrease in cell volume, similar to that reported for somatic cells. Regulatory volume increase (RVI), a complementary process which is assumed to occur following initial shrinkage of sperm volume after exposure to a hypertonic medium, has not yet been described in detail for spermatozoa. In this study, we investigated whether spermatozoa are able to regulate their volume after hypertonic stress and whether this ability is maintained in preserved sperm. Cell volume changes were recorded using electronic cell sizing. Sperm response to the ion channels blockers quinidine, tamoxifen, and dydeoxyforskolin, and to protein kinase/phosphatase inhibitors lavendustin, staurosporine, and vanadate was studied to investigate possible mechanisms of RVI. Annexin V staining was used in combination with propidium iodide to determine whether hypertonic stress may induce apoptosis. Overall protein tyrosine phosphorylation under hypertonic conditions was measured via flow cytometry using antiphosphotyrosine antibody. Spermatozoa exposed to hypertonic stress initially responded with an abundant subpopulation according to the perfect osmometer model and recovered their volume from this shrinkage after 20 min. RVI was inhibited by quinidine and tamoxifen, which indicates the involvement of the important cellular ions sodium and chloride in this process. Volume regulatory ability was essentially maintained during storage of liquid semen. However, the response of the sperm population was heterogeneous. A second population raised, containing spermatozoa with larger volumes, which demonstrated irregularities in the volume response with respect to osmotic challenge, ion channel blockers, and storage. Under hypertonic conditions, both protein kinase inhibitors (PKI) led to increased isotonic volumes and to elevated initial relative volumes and subsequent volume decrease. RVI was inhibited by the vanadate. Hypertonic stress did not result in an increase in early apoptotic cells, but produced a shift toward late necrotic cells. Substitution of sodium and chloride by choline and sulfate resulted in decreased isotonic volume of sperm treated with lavendustin. Tyrosine phosphorylation levels were reduced after 20 min under hypertonic conditions. It was concluded that RVI is regulated via a protein tyrosine kinase-dependent pathway, and that dephosphorylation occurs when volume regulation is required. The necrotic volume increase (NVI) is associated with the accumulation of sodium and chloride following uncontrolled opening of the channels. The ability to regulate volume after exposure to hypertonic conditions is important for sperm functionality and can have practical applications in spermatological diagnostics and cryopreservation.

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Section: Discussionsupporting

confidence: 89%

Regulatory and necrotic volume increase in boar spermatozoa

Petrunkina

Jebe

Töpfer‐Petersen

2005

Journal Cellular Physiology

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“…Ϫ transport during RVD (9,16,28,39) have already been suggested in previous experiments. This is shown to be the case in the present study because RVD was insensitive to Na ϩ suppression and was inhibited by external Cl Ϫ removal.…”

Section: Discussionsupporting

confidence: 66%

“…Ϫ in RVD was also clearly established in different epithelial-derived cells (28,36). However, although most of the authors agree with the observation that the presence of HCO 3…”

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confidence: 88%

Extracellular pH alkalinization by Cl⁻/HCO₃⁻exchanger is crucial for TASK2 activation by hypotonic shock in proximal cell lines from mouse kidney

L’Hoste¹,

Barrière²,

Belfodil³

et al. 2007

American Journal of Physiology-Renal Physiology

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We have previously shown that K(+)-selective TASK2 channels and swelling-activated Cl(-) currents are involved in a regulatory volume decrease (RVD; Barriere H, Belfodil R, Rubera I, Tauc M, Lesage F, Poujeol C, Guy N, Barhanin J, Poujeol P. J Gen Physiol 122: 177-190, 2003; Belfodil R, Barriere H, Rubera I, Tauc M, Poujeol C, Bidet M, Poujeol P. Am J Physiol Renal Physiol 284: F812-F828, 2003). The aim of this study was to determine the mechanism responsible for the activation of TASK2 channels during RVD in proximal cell lines from mouse kidney. For this purpose, the patch-clamp whole-cell technique was used to test the effect of pH and the buffering capacity of external bath on Cl(-) and K(+) currents during hypotonic shock. In the presence of a high buffer concentration (30 mM HEPES), the cells did not undergo RVD and did not develop outward K(+) currents (TASK2). Interestingly, the hypotonic shock reduced the cytosolic pH (pH(i)) and increased the external pH (pH(e)) in wild-type but not in cftr (-/-) cells. The inhibitory effect of DIDS suggests that the acidification of pH(i) and the alkalinization of pH(e) induced by hypotonicity in wild-type cells could be due to an exit of HCO(3)(-). In conclusion, these results indicate that Cl(-) influx will be the driving force for HCO(3)(-) exit through the activation of the Cl(-)/HCO(3)(-) exchanger. This efflux of HCO(3)(-) then alkalinizes pH(e), which in turn activates TASK2 channels.

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“…The relatively minor role of acid-transporting pathways in RVD is also underscored by the lack of any effect of Na ϩ /H ϩ exchange inhibition on volume recovery. Although this may be typical for many cells, activation of Na ϩ /H ϩ exchange upon swelling has in fact been observed in certain cell types (46) and under certain conditions (51).…”

Section: Discussionmentioning

confidence: 98%

Importance of cytoskeletal elements in volume regulatory responses of trout hepatocytes

Ebner¹,

Cordas²,

Pafundo³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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The role of cytoskeletal elements in volume regulation was studied in trout hepatocytes by investigating changes in F-actin distribution during anisotonic exposure and assessing the impact of cytoskeleton disruption on volume regulatory responses. Hypotonic challenge caused a significant decrease in the ratio of cortical to cytoplasmic F-actin, whereas this ratio was unaffected in hypertonic saline. Disruption of microfilaments with cytochalasin B (CB) or cytochalasin D significantly slowed volume recovery following hypo- and hypertonic exposure in both attached and suspended cells. The decrease of net proton release and the intracellular acidification elicited by hypotonicity were unaltered by CB, whereas the increase of proton release in hypertonic saline was dramatically reduced. Because amiloride almost completely blocked the hypertonic increase of proton release and cytoskeleton disruption diminished the associated increase of intracellular pH (pH(i)), we suggest that F-actin disruption affected Na(+)/H(+) exchanger activity. In line with this, pH(i) recovery after an ammonium prepulse was significantly inhibited in CB-treated cells. The increase of cytosolic Na(+) under hypertonic conditions was not diminished but, rather, enhanced by F-actin disruption, presumably due to inhibited Na(+)-K(+)-ATPase activity and stimulated Na(+) channel activity. The elevation of cytosolic Ca(2+) in hypertonic medium was significantly reduced by CB. Altogether, our results indicate that the F-actin network is of crucial importance in the cellular responses to anisotonic conditions, possibly via interaction with the activity of ion transporters and with signalling cascades responsible for their activation. Disruption of microtubules with colchicine had no effect on any of the parameters investigated.

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The role of bicarbonate in regulatory volume decrease (RVD) in the epithelial-derived human breast cancer cell line ZR-75-1

Cited by 13 publications

References 25 publications

Regulatory and necrotic volume increase in boar spermatozoa

Regulatory and necrotic volume increase in boar spermatozoa

Extracellular pH alkalinization by Cl⁻/HCO₃⁻exchanger is crucial for TASK2 activation by hypotonic shock in proximal cell lines from mouse kidney

Importance of cytoskeletal elements in volume regulatory responses of trout hepatocytes

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The role of bicarbonate in regulatory volume decrease (RVD) in the epithelial-derived human breast cancer cell line ZR-75-1

Cited by 13 publications

References 25 publications

Regulatory and necrotic volume increase in boar spermatozoa

Regulatory and necrotic volume increase in boar spermatozoa

Extracellular pH alkalinization by Cl−/HCO3−exchanger is crucial for TASK2 activation by hypotonic shock in proximal cell lines from mouse kidney

Importance of cytoskeletal elements in volume regulatory responses of trout hepatocytes

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Extracellular pH alkalinization by Cl⁻/HCO₃⁻exchanger is crucial for TASK2 activation by hypotonic shock in proximal cell lines from mouse kidney