2014
DOI: 10.1182/blood-2014-05-572024
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Hemolysis is a primary ATP-release mechanism in human erythrocytes

Abstract: The hypothesis that regulated ATP release from red blood cells (RBCs) contributes to nitric oxide-dependent control of local blood flow has sparked much interest in underlying release mechanisms. Several stimuli, including shear stress and hypoxia, have been found to induce significant RBC ATP release attributed to activation of ATP-conducting channels. In the present study, we first evaluated different experimental approaches investigating stimulated RBC ATP release and quantifying hemolysis. We then measured… Show more

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Cited by 95 publications
(88 citation statements)
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“…Although we began with the hypothesis that regulated ATP release mechanisms do operate in RBCs, after extensively verifying each experimental approach, we came to the conclusion expressed in the title: ie, that "Hemolysis is a primary ATP release mechanism in human erythrocytes." 1 In the course of the study, while attempting to reproduce previously published findings, we identified a number of methodological pitfalls (the major ones are discussed in the supplemental Methods available on Blood Web site), which likely precluded a proper evaluation of ATP release and also the contribution of hemolysis in the earlier studies 2-10 cited by Kirby et al We agree that "liberation of ATP secondary to hemolysis is not mutually exclusive of regulated export." 11 Our point is that without the controls described in our paper, a confounding effect of hemolysis cannot be excluded.…”
Section: Hemolysis Is a Primary And Physiologically Relevant Atp Relementioning
confidence: 79%
“…Although we began with the hypothesis that regulated ATP release mechanisms do operate in RBCs, after extensively verifying each experimental approach, we came to the conclusion expressed in the title: ie, that "Hemolysis is a primary ATP release mechanism in human erythrocytes." 1 In the course of the study, while attempting to reproduce previously published findings, we identified a number of methodological pitfalls (the major ones are discussed in the supplemental Methods available on Blood Web site), which likely precluded a proper evaluation of ATP release and also the contribution of hemolysis in the earlier studies 2-10 cited by Kirby et al We agree that "liberation of ATP secondary to hemolysis is not mutually exclusive of regulated export." 11 Our point is that without the controls described in our paper, a confounding effect of hemolysis cannot be excluded.…”
Section: Hemolysis Is a Primary And Physiologically Relevant Atp Relementioning
confidence: 79%
“…Hence, the mechanism of ETX-induced hemolysis is different from those of HlyA- and leukotoxin A-induced hemolysis. It was also reported that hemolysis is a primary ATP-release mechanism in human erythrocytes stimulated by several stimuli, including shear stress and hypoxia [37].
10.1080/21505594.2018.1528842-F0008Figure 8.Inferred model for ETX-induced hemolysis.
…”
Section: Discussionmentioning
confidence: 99%
“…Однією з причин зниження стійкості до кислотного гемолізу є наявність у еритроцитів старих тварин оксидативно/нітрозативного стресу, тобто підвищеної генерації супероксиду (O 2 -) і над-лишкового оксиду азоту (NO) [2]. Відомо, що при гемолізі еритроцитів звільняється АТФ [3], який активує ендотеліальну NO-синтазу (еNOS) [4], але руйнування пламатичної мембрани еритроцитів (гемоліз) і звільнен-ня гемоглобіну має за наслідок утворення газового трансмітера оксиду вуглецю (СО) через руйнування гему гемоксидазою [5], так і сприяє підвищенню синтезу гемоглобіну [6]. В еритроцитах інтенсивно синтезується не лише NO при відновленні нітрит-аніона (NO 2 -) дезоксигемоглобіном [7], але і H 2 S ферментом меркаптопіруватсульфотранс-феразою (MPST) [8].…”
Section: вступunclassified