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Reduction of Erythrocyte (RBC) Deformability Attenuates Low Oxygen Tension (pO 2 ) Induced ATP Release from the RBC
Author(s) -
Sridharan Meera,
Adderley Shaquria,
Hanson Madelyn,
Bowles Elizabeth,
Stephenson Alan,
Sprague Randy
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.767.11
Subject(s) - chemistry , incubation , erythrocyte deformability , red blood cell , biophysics , cytoskeleton , adenosine triphosphate , biochemistry , cell , biology
The mechanism by which decreased pO 2 stimulates ATP release from RBCs has not been established. Here we evaluated the hypothesis that RBC deformability is required for ATP release from rabbit RBCs in response to exposure to low pO 2 . Deformability of RBCs, measured with a St. George's Blood Filtrometer, was decreased by incubation of RBCs with diamide, an agent that promotes cytoskeletal cross‐linking. Incubation of RBCs with diamide (100 uM) resulted in a 7.67 ± 1.19 % reduction in RBC deformability by 30 min that was stable for 1 hr (n=4). In untreated RBCs, changes in pO 2 from 121.9 ± 2.7 to 13.7 ± 1.2 mmHg resulted in a significant 8.5 ± 2.9 fold increase in ATP release (p<0.01, n=5). In contrast, in diamide treated RBCs, changes of pO 2 from 125.8 ± 6.1 to 13.5 ± 0.6 mmHg resulted in only a 2.9 ± 1.0 fold increase in ATP release, which was significantly lower than the increase in untreated RBCs (p<0.05, n=5). To ensure that effects of diamide on low pO 2 ‐induced ATP release were selective for that signaling pathway and was not due to a general inhibition of ATP release, RBCs were incubated with iloprost (ILO), to stimulate ATP release in the absence or presence of diamide. Diamide did not inhibit ILO‐induced ATP release (n=2). These results are consistent with the hypothesis that membrane deformability is required for low pO 2 ‐induced ATP release from rabbit RBCs. (ADA grant RA‐133 and NIH grants HL‐64180 & HL‐89094)