Diagnostische Verfahren

Rick, W.

doi:10.1007/978-3-642-66136-5_4

Cited by 1 publication

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References 32 publications

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“…Besides the release of amino acids that can contribute to the anion loss, an exit of HCO 3 3 generated within the cells is possible. An exit of cellular HCO 3 3 in response to hypotonicity can explain the pH i acidi¢cation during RVD and has been demonstrated in renal cells [15,16], Ehrlich ascites tumor cells [4] and human promyelocytic leukemic HL-60 cells [12]. There are two possible routes for the exit of intracellular HCO 3 3 : (i) through the volume-sensitive anion channel with a permeability ratio (HCO 3 3 /Cl 3 ) of 0.6 [17]; (ii) via an AE.…”

Section: Discussionmentioning

confidence: 92%

Anion exchanger isoform 2 operates in parallel with Na⁺/H⁺ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells

et al. 2002

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Intracellular pH (pH i ) homeostasis was investigated in human cervical cancer SiHa cells undergoing regulatory volume decrease (RVD) to determine which transport systems were involved. Using isoform-specific primers, mRNA transcripts of Na + /H + exchanger isoform 1 (NHE1) and isoform 3 were identified by reverse transcriptase polymerase chain reaction (RT-PCR) and the results confirmed by Western immunoblotting. From anion exchanger isoforms 1^3 (AE1^3), only the mRNA transcript of AE2 was identified by RT-PCR and the identity was confirmed by digestion with a specific restriction endonuclease. SiHa cells loaded with the fluorescent dye 2P P,7P Pbis(carboxyethyl)-5(6)-carboxyfluorescein and resuspended in isotonic media showed a stable pH i . In contrast, a gradual internal acidification took place following resuspension in hypotonic media. The NHE inhibitors, HOE694 (10 W WM) and amiloride (1 mM), showed a similar potency in enhancing the rate and extent of the hypotonicity-induced internal acidification. The absence of extracellular Na + also substantially enhanced the acidification during RVD. These results suggest that internal acidification during RVD is mainly compensated by the operation of NHE1. Extracellular Cl 3 was critically necessary for the pH i acidification during RVD. The hypotonicity-induced acidification was significantly attenuated by 100 W WM 4,4P Pdiisothiocyanostilbene-2,2P P-disulfonic acid, a concentration inhibiting more than 90% AE activity. This indicates that AE2 mediates a net Cl 3 influx with compensating HCO 3 3 efflux during RVD. We conclude that AE2 operates in parallel with NHE1 to regulate pH i during RVD of human cervical cancer cells. ß 2002 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.

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Section: Discussionmentioning

confidence: 92%

Anion exchanger isoform 2 operates in parallel with Na⁺/H⁺ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells

et al. 2002

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show abstract

Diagnostische Verfahren

Cited by 1 publication

References 32 publications

Anion exchanger isoform 2 operates in parallel with Na⁺/H⁺ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells

Anion exchanger isoform 2 operates in parallel with Na⁺/H⁺ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells

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Diagnostische Verfahren

Cited by 1 publication

References 32 publications

Anion exchanger isoform 2 operates in parallel with Na+/H+ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells

Anion exchanger isoform 2 operates in parallel with Na+/H+ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells

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Anion exchanger isoform 2 operates in parallel with Na⁺/H⁺ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells

Anion exchanger isoform 2 operates in parallel with Na⁺/H⁺ exchanger isoform 1 during regulatory volume decrease of human cervical cancer cells