Increased Immunogenicity of Human Renal Carcinoma Cells
following Treatment with Cholesterol Derivatives

Ludes, Bertrand; Staedel, Cathy; Jacqmin, Didier; Crémel, Gérard; Hubert, P.; Bollack, C; Beck, Jean-Paul

doi:10.1159/000464027

Cited by 2 publications

(3 citation statements)

References 17 publications

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“…This is consistent with the decreased membrane fluidity in the presence of an increased membrane cholesterol content reported in a number of cell lines including akata cells (lymphoid cell line), human umbilical vein endothelial cells, rat aortic smooth cells, guinea pig keratinocytes, human renal carcinoma cells, and rat prostatic epithelial cells. 7,[25][26][27][28][29][30] In the present studies, the increase in cholesterol concentration produced a reduction of sodium-dependent sulfate uptake in cells in a concentration-dependent manner due to a reduction in the V max of sodium/sulfate cotransport in MDCK cells transfected with NaSi-1. Levi et al 8 also reported a decreased V max for sodium/phosphate cotransport with no change in K m in the BBM isolated from aged rats which exhibit a decrease in BBM fluidity and an increase in BBM cholesterol content.…”

Section: Discussionsupporting

confidence: 50%

Modulation of sulfate renal transport by alterations in cell membrane fluidity

Lee

Balasubramanian

Murer

et al. 1999

Journal of Pharmaceutical Sciences

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Changes in membrane fluidity have been shown to alter the sodium-dependent renal transport of glucose and phosphate; however, this has not been examined for sodium/sulfate cotransport in the renal proximal tubule. Sodium/sulfate cotransport regulates the homeostasis of sulfate in mammals. The objective of this study was to investigate the influence of alterations of membrane fluidity on sodium-coupled sulfate transport in the Madin-Darby canine kidney cells, which have been stably transfected with sodium/sulfate cotransporter (NaSi-1) cDNA (MDCK-Si). Preincubation of cells with 0. 2 mM cholesterol significantly decreased the V(max) for sodium/sulfate cotransport (13.69 +/- 1.11 vs 10.15 +/- 1.17 nmol/mg protein/5 min, mean +/- SD, n = 4, p < 0.01) with no significant alteration in K(m). The addition of benzyl alcohol (20 mM) to cells increased the V(max) of sulfate uptake by 20% (11.97 +/- 0.91 vs 14. 35 +/- 0.56 nmol/mg protein/5 min, mean +/- SD, n = 3, p < 0.05) with no significant change in K(m). Membrane fluidity, as measured by the fluorescence polarization of 1,6-diphenyl 1,3,5-hexatriene (DPH), was significantly increased in MDCK-Si cells treated with 20 mM benzyl alcohol and decreased in the cells preincubated with 0.2 mM cholesterol, compared with control cells. Our results suggest that alterations in membrane fluidity that may occur as a result of disease states, aging, and pregnancy may play an important role in the modulation of renal sodium/sulfate cotransport.

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Section: Discussionsupporting

confidence: 50%

Modulation of sulfate renal transport by alterations in cell membrane fluidity

Lee

Balasubramanian

Murer

et al. 1999

Journal of Pharmaceutical Sciences

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“…In contrast to previous find ings, measurements of membrane fluidity did not clearly establish the causal relationship between increased immunogenicity and decreased fluidity due to stiffening of the tumor cell membranes [ 18],…”

Section: Discussioncontrasting

confidence: 99%

“…The present study was conducted on cells isolated from hu man renal carcinoma biopsies, in which we previously demonstrated that treatment by some cholesterol deriva tives induced increased immunogenicity [ 18]. To perform multiple and repeated experiments over a long time inter val and to be sure to study a homogeneous cell popula tion, we adapted human renal carcinoma cells to monolayer growth in vitro.…”

Section: Introductionmentioning

confidence: 99%