Stimulation of calcium influx and CK1α by NF‐κB antagonist [6]‐Gingerol reprograms red blood cell longevity

Author(s):  
Hassan S. Alamri ◽  
Jawaher Alsughayyir ◽  
Maaged Akiel ◽  
Yazeed A. Al‐Sheikh ◽  
Ahmed M. Basudan ◽  
...  
Nature ◽  
1972 ◽  
Vol 239 (5372) ◽  
pp. 399-401 ◽  
Author(s):  
A. I. M. GLEN ◽  
M. W. B. BRADBURY ◽  
JANET WILSON

1985 ◽  
Vol 227 (1) ◽  
pp. 105-112 ◽  
Author(s):  
L Neyses ◽  
R Locher ◽  
M Stimpel ◽  
R Streuli ◽  
W Vetter

To study the effect of cholesterol and its pathophysiologically important oxidized derivatives (OSC) on the calcium entry channel, the human red blood cell was used as a model system. The calcium ejecting adenosinetriphosphatase (ATPase) was inhibited by vanadate. The cells were loaded with OSC at concentrations between 1.25 × 10(-5) and 25 × 10(-5) mol/l. 22-Hydroxycholesterol, cholestan-3 beta,5 alpha,6 beta-triol, 5 alpha-cholestan-3 beta-ol,3 beta,5 alpha-dihydroxycholestan-6-one and 3 beta-hydroxy-5 alpha-cholestan-7-one stimulated 45Ca2+ influx by up to almost 90%, whereas 25-hydroxycholesterol, 7 beta-hydroxycholesterol, 20 alpha-hydroxycholesterol and 7-oxocholesterol inhibited influx by up to 75%. Both stimulation and inhibition were dependent on the amount of OSC incorporated into the membrane. More than 90% of the total modification of calcium influx by OSC was accounted for by an influence on the nitrendipine-inhibitable part of influx. Enrichment of cholesterol in the membrane greatly stimulated, and cholesterol depletion inhibited, Ca2+ influx. These results demonstrate that cholesterol and its oxidized derivatives are able to modulate the calcium channel in human red blood cells in a highly stereospecific manner.


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