The pH dependence of the cardiac sarcolemmal Ca2+-transporting ATPase: evidence that the Ca2+ translocator bears a doubly negative charge

Dixon, Deborah A.; Haynes, Duncan H.

doi:10.1016/0005-2736(90)90164-j

Cited by 23 publications

(13 citation statements)

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“…In vascular smooth muscle the activity of the SR Ca2+-ATPase is modulated by pH, to the point that proton countertransport causes this enzyme to function as a Ca2+/H' exchanger (13)(14)(15). To distinguish Ca2+/H+ exchange across the plasma membrane from that occurring at the level of the SR, Ca,2+ was monitored while the concentration of external protons was altered acutely.…”

Section: Discussionmentioning

confidence: 99%

“…There is now evidence for multiple subtypes of Ca2+-ATPases present in intracellular organelles and in the plasma membrane (9)(10)(11)(12). It is well known that the sarcoplasmic reticulum (SR) Ca,2+ -ATPase acts as a Ca2+/H+ exchanger (13)(14)(15). A plasma membrane Cai2+-ATPase, originally characterized in bovine aorta by Furukawa and Nakamura (16), is the main cell calcium extrusion mechanism in vascular smooth muscle.…”

Section: Introductionmentioning

confidence: 99%

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Intracellular acidification associated with changes in free cytosolic calcium. Evidence for Ca2+/H+ exchange via a plasma membrane Ca(2+)-ATPase in vascular smooth muscle cells.

Daugirdas

Arrieta²,

Ye³

et al. 1995

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intracellular acidification associated with changes in free cytosolic calcium. Evidence for Ca2+/H+ exchange via a plasma membrane Ca(2+)-ATPase in vascular smooth muscle cells.

Daugirdas

Arrieta²,

Ye³

et al. 1995

J. Clin. Invest.

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“…of seven experiments for each condition. *P õ 0.05 for the following conditions: (a) bafilomycin treated versus Gillies et al, 1992) Kentish, 1990), or by inhibition of d1070) exhibit not only a lost in their metastatic potential (Chu et al, 1991), but also a much lower either the PM-or ER-Ca 2/ -ATPase (Carafoli, 1987;Dixon and Haynes, 1990;Lytton et al, 1992 in levels (Lax et al, 1994;. of tumor cells correlates positively with the levels of expression of dual intermediate filaments (Ben-ze'ev et These various responses are cell type specific and they seem to be also related to the metabolic status of the al., 1986; Trask et al, 1990;Hendrix et al, 1992;Chu et al, 1996).…”

Section: C8161-d1070 Cells (Cd) Were Obtained By Transfection Of C8161mentioning

confidence: 96%

“…trobon et al, 1990;Gillies et al, 1992 ] in in proliferation may be distinct from its effects in tumorigenicity and metastasis. channels (Dixon and Haynes, 1990;Lytton et al, 1992).…”

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confidence: 95%

Distinct regulation of pHin and [Ca2+]in in human melanoma cells with different metastatic potential

et al. 1998

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We investigated whether alterations in the mechanisms involved in intracellular pH (pHin) and intracellular calcium ([Ca2+]in) homeostasis are associated with the metastatic potential of poorly (A375P) and highly (C8161) metastatic human melanoma cells. We monitored pHin and [Ca2+]in simultaneously, using the fluorescence of SNARF-1 and Fura-2, respectively. Our results indicated that steady-state pHin and [Ca2+]in between these cell types were not significantly different. Treatment of cells with NH4Cl resulted in larger pHin increases in highly than in poorly metastatic cells, suggesting that C8161 cells have a lower H+ buffering capacity than A375P. NH4Cl treatment also increased [Ca2+]in only in C8161 cells. To determine if the changes in [Ca2+]in triggered by NH4Cl treatment were due to alterations in either H+- or Ca2+-buffering capacity, cells were treated with the Ca2+-ionophore 4Br-A23187, to alter [Ca2+]in. The magnitude of the ionophore-induced [Ca2+]in increase was slightly greater in C8161 cells than in A375P. Moreover, A375P cells recover from the ionophore-induced [Ca2+]in load, whereas C8161 cells did not, suggesting that A375P may exhibit distinct [Ca2+]in regulatory mechanisms than C8161 cells, to recover from Ca2+ loads. Removal of extracellular Ca2+ ([Ca2+]ex) decreased [Ca2+]in in both cell types at the same extent. Ionophore treatment in the absence of [Ca2+]ex transiently increased [Ca2+]in in C8161, but not in A375P cells. Endoplasmic reticulum (ER) Ca2+-ATPase inhibitors such as cyclopiazonic acid (CPA) and thapsigargin (TG) increased steady-state [Ca2+]in only in C8161 cells. Together, these data suggest that the contribution of intracellular Ca2+ stores for [Ca2+]in homeostasis is greater in highly than in poorly metastatic cells. Bafilomycin treatment, to inhibit V-type H+-ATPases, corroborated our previous results that V-H+-ATPases are functionally expressed at the plasma membranes of highly metastatic, but not in poorly metastatic cells (Martínez-Zaguilán et al., 1993). Collectively, these data suggest that distinct pHin and [Ca2+]in regulatory mechanisms are present in poorly and highly metastatic human melanoma cells.

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“…endoplasmic reticulum Ca2+-ATPases, Ca2+ channels, Na+/Ca2+ exchanger, and Ca2+-binding proteins [ 13]. Since pH can affect any of these systems [14,15], changes in pH,n can alter Ca2+ homeostasis.…”

Section: Introductionmentioning

confidence: 99%

[Ca2+]i and pHin Homeostasis in Kaposi Sarcoma Cells

Martı́nez-Zaguilán¹,

Chinnock²,

Waldhopkins³

et al. 1996

Cell Physiol Biochem

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Changes in intracellular pH (pH_in) and intracellular calcium concentration [Ca²⁺]_i play a major role in signal transduction leading to cell growth, differentiation and transformation. In some tumor cell lines, vacuolar (V-type) H⁺-adenosine triphosphatases (ATPases) are important in pH_in regulation. To clarify the neoplastic nature and endothelial origin of Kaposi sarcoma (KS), pH_in and [Ca²⁺]_i and the functional expression of V-type H⁺-ATPases were evaluated in cultured endothelial marker-positive KS cells derived from AIDS-KS skin lesions as compared to human umbilical vein endothelial cells (HUVEC). Human skin fibroblasts (HSF) were also examined. Cells were examined using fluorescence spectroscopy with the pH_in indicator SNARF-1 and the [Ca²⁺]i indicator Fura-2. We found that whereas pH_in recovery from acid loading occurred in the absence of Na⁺ and HCO^–₃ in HUVEC and HSF, KS cells did not recover. Moreover, removal of extracellular Na⁺ had no effect on [Ca²⁺]_i in HUVEC, but transiently increased [Ca²⁺]_i in KS cells and HSF. This [Ca²⁺]_i spike was unaffected by Ca²⁺-free medium, suggesting that it is not due to Na⁺/Ca²⁺ exchange. In addition, use of K⁺-containing and K⁺-free medium to mimic depolarization or hyperpolarization, which may occur during Na⁺ removal, did not cause [Ca²⁺]_i changes. The [Ca²⁺]_i levels were also not sensitive to intracellular acidification but were specifically sensitive to [Na⁺]. Thus, KS cells differ from normal endothelial cells in the kinetics of pH_in recovery to acid loads, and in the presence of a specific [Na⁺]-sensitive intracellular Ca²⁺ pool. These differences in ion homeostasis indicate that these cell types are not developmentally related or that alterations in ion transport are a part of the etiology of the KS lesion.

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The pH dependence of the cardiac sarcolemmal Ca2+-transporting ATPase: evidence that the Ca2+ translocator bears a doubly negative charge

Cited by 23 publications

References 47 publications

Intracellular acidification associated with changes in free cytosolic calcium. Evidence for Ca2+/H+ exchange via a plasma membrane Ca(2+)-ATPase in vascular smooth muscle cells.

Intracellular acidification associated with changes in free cytosolic calcium. Evidence for Ca2+/H+ exchange via a plasma membrane Ca(2+)-ATPase in vascular smooth muscle cells.

Distinct regulation of pHin and [Ca2+]in in human melanoma cells with different metastatic potential

[Ca<sup>2+</sup>]<sub>i</sub> and pH<sub>in</sub> Homeostasis in Kaposi Sarcoma Cells

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