[Ca2+](i) and pH(in) homeostasis in Kaposi sarcoma cells

Raul Martínez-Zaguilán, Brian F. Chinnock, Sarah Wald-Hopkins, Michael J Bernas, Dennis Way, Martin E Weinand, Marlys H Witte, Robert J. Gillies

Research output: Contribution to journalArticle

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Abstract

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 HCO3- 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.

Original languageEnglish (US)
Pages (from-to)169-184
Number of pages16
JournalCellular Physiology and Biochemistry
Volume6
Issue number3
StatePublished - 1996

Fingerprint

Kaposi's Sarcoma
Homeostasis
Human Umbilical Vein Endothelial Cells
Skin
Fibroblasts
Adenosine Triphosphatases
Acids
Fura-2
Fluorescence Spectrometry
Ion Transport
Tumor Cell Line
Cell Differentiation
Signal Transduction
Acquired Immunodeficiency Syndrome
Endothelial Cells
Ions
Calcium
Growth

Keywords

  • [Ca](i)
  • Endothelial cells
  • Fluorescence
  • Fura-2
  • Human skin fibroblasts
  • Kaposi sarcoma
  • Na/Ca exchange
  • Na/H exchange
  • pH(in)
  • SNARF-1

ASJC Scopus subject areas

  • Cell Biology
  • Physiology

Cite this

Martínez-Zaguilán, R., Chinnock, B. F., Wald-Hopkins, S., Bernas, M. J., Way, D., Weinand, M. E., ... Gillies, R. J. (1996). [Ca2+](i) and pH(in) homeostasis in Kaposi sarcoma cells. Cellular Physiology and Biochemistry, 6(3), 169-184.

[Ca2+](i) and pH(in) homeostasis in Kaposi sarcoma cells. / Martínez-Zaguilán, Raul; Chinnock, Brian F.; Wald-Hopkins, Sarah; Bernas, Michael J; Way, Dennis; Weinand, Martin E; Witte, Marlys H; Gillies, Robert J.

In: Cellular Physiology and Biochemistry, Vol. 6, No. 3, 1996, p. 169-184.

Research output: Contribution to journalArticle

Martínez-Zaguilán, R, Chinnock, BF, Wald-Hopkins, S, Bernas, MJ, Way, D, Weinand, ME, Witte, MH & Gillies, RJ 1996, '[Ca2+](i) and pH(in) homeostasis in Kaposi sarcoma cells', Cellular Physiology and Biochemistry, vol. 6, no. 3, pp. 169-184.
Martínez-Zaguilán R, Chinnock BF, Wald-Hopkins S, Bernas MJ, Way D, Weinand ME et al. [Ca2+](i) and pH(in) homeostasis in Kaposi sarcoma cells. Cellular Physiology and Biochemistry. 1996;6(3):169-184.
Martínez-Zaguilán, Raul ; Chinnock, Brian F. ; Wald-Hopkins, Sarah ; Bernas, Michael J ; Way, Dennis ; Weinand, Martin E ; Witte, Marlys H ; Gillies, Robert J. / [Ca2+](i) and pH(in) homeostasis in Kaposi sarcoma cells. In: Cellular Physiology and Biochemistry. 1996 ; Vol. 6, No. 3. pp. 169-184.
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