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

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Abstract
Changes in intracellular pH (pHin) 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 pHin regulation. To clarify the neoplastic nature and endothelial origin of Kaposi sarcoma (KS), pHin 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 pHin indicator SNARF-1 and the [Ca2+]i indicator Fura-2. We found that whereas pHin 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 pHin 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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