Periods without agitation diminish platelet mitochondrial function during storage

Skripchenko, Andrey; Myrup, Andrew; Thompson-Montgomery, Dedeene; Awatefe, Helen; Moroff, Gary; Wagner, Stephen J.

doi:10.1111/j.1537-2995.2009.02450.x

Cited by 42 publications

(71 citation statements)

References 37 publications

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“…Superoxide anion production was determined using dihydroethidium (DHE; Invitrogen), which is oxidized by superoxide to fluorescent ethidium. For analysis, platelets were diluted to 1 × 10 6 cells/ml in phosphate-buffered saline (PBS) supplemented with 0.1% human plasma and stained with 5 mmol/l CM-H 2 DCFDA or 5 mmol/l DHE for 20 min at 37 °C, as previously described [29]. Fluorescence was detected by flow cytometry.…”

Section: Methodsmentioning

confidence: 99%

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-κB Activation

Johnson¹,

Marks²

2015

Transfus Med Hemother

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Background: Pathogen inactivation (PI) technologies for platelets aim to improve transfusion safety by preventing the replication of contaminating pathogens. However, as a consequence of treatment, aspects of the platelet storage lesion are amplified. Mirasol treatment also affects platelet signal transduction and apoptotic protein expression. The aim of this study was to examine the effect of Mirasol treatment on the generation of reactive oxygen species (ROS) and subsequent oxidative stress. Methods: Pooled platelet concentrates were prepared in platelet-additive solution (70% SSP+ / 30% plasma). ABO-matched platelets were pooled and split, and treated with the Mirasol system (TerumoBCT) or left untreated as a control. Platelet samples were tested on day 1, 5, and 7 post-collection. Results: Mirasol-treated platelets had increased formation of ROS by day 5 of storage. Oxidative damage, in the form of protein carbonylation, was higher in Mirasol-treated platelets, whilst no effect on nitrotyrosine formation or lipid peroxidation was detected. The NF-κB signaling pathway was also activated in Mirasol-treated platelets, with increased expression and phosphorylation of NF-κB p65 and IκBa. Conclusion: These data demonstrate that Mirasol-treated platelets produce more ROS and display protein alterations consistent with oxidative damage.

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Section: Methodsmentioning

confidence: 99%

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-κB Activation

Johnson¹,

Marks²

2015

Transfus Med Hemother

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“…Because mitochondria utilize oxygen to synthesize nearly 95% of the adenosine triphosphate (ATP) required to meet the body's energy needs, impaired perfusion during hemorrhagic shock results in mitochondrial and energetic stress (6); Although resuscitation can restore adequate tissue oxygen levels, reperfusion may exacerbate mitochondrial dysfunction by increasing the generation of reactive oxygen species (ROS) (5). ROS not only directly damage mitochondrial proteins, but they can also promote the formation of the mitochondrial permeability transition pore, increase release of cytochrome c, and enhance apoptosis (7). Despite adequate resuscitation following hemorrhagic shock, persistent mitochondrial dysfunction may contribute to ongoing cellular injury and organ failure (8).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Rescues Kidney Mitochondrial Function Following Hemorrhagic Shock

Wang

Guan

et al. 2014

Journal of Surgical Research

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“…This has been achieved with the use of platelet activation inhibitors (NO, phosphodiesterase inhibitors, apyrase and prostacyclin, protease inhibitors), [50][51][52][53][54][55][56][57] through inclusion of additives such as acetate, phosphate, gluconate, potassium, and magnesium 41,[43][44][45][46][47][58][59][60] and through the implementation of modified storage bags with agitation. 61 However, these measures have provided only modest improvements in platelet viability. This may not be surprising given that these approaches only partially mitigate the consequences of mitochondria damage, and do not target the primary underlying cause of the PSL, namely irreversible mitochondrial injury.…”

Section: Apoptotic and Necrotic Death Pathways: Implications For The mentioning

confidence: 99%

Procoagulant platelets: are they necrotic?

Jackson

Schoenwaelder

2010

Blood

143

141

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Apoptosis and necrosis represent distinct cell death processes that regulate mammalian development, physiology and disease. Apoptosis characteristically leads to the silent destruction and removal of cells in the absence of an inflammatory response. In contrast, necrotic cell death can induce physiologic inflammatory responses linked to tissue defense and repair. Although anucleate, platelets undergo programmed cell death, with apoptosis playing an important role in clearing effete platelets from the circulation. While it has long been recognized that procoagulant platelets exhibit characteristic features of dying cells, recent studies have demonstrated that platelet procoagulant function can occur independent of apoptosis. A growing body of evidence suggest that the biochemical, morphologic and functional changes underlying agonist-induced platelet procoagulant function are broadly consistent with cell necrosis, raising the possibility that distinct death pathways regulate platelet function and survival. In this article, we will discuss the mechanisms underlying apoptotic and necrotic cell death pathways and examine the evidence linking these pathways to the platelet procoagulant response. We will also discuss the potential contribution of these pathways to the platelet storage lesion and propose a simplified nomenclature to describe procoagulant platelets. IntroductionUntil the early 1970s it was thought that all cells die as a result of necrosis (Table 1); a form of cell death that is prominent when tissues undergo extensive damage from trauma or disease. This concept changed dramatically in 1972 after the landmark observations of Kerr and colleagues, 9 who described a new form of cell death, termed apoptosis (Table 1). Since then, the genetic and biochemical processes responsible for apoptotic cell death have been extensively investigated. It is now well defined that apoptosis is a key process underlying human development, normal physiology and a range of common human diseases. 10 In contrast, the concepts underlying necrosis have become less clear-cut. While it has long been assumed that necrosis is predominantly a pathologic process resulting from tissue injury, there is growing evidence that cells can orchestrate their own demise through programmed cell necrosis in a manner that initiates physiologic inflammatory and repair responses. [2][3][4][6][7][8] Although anucleate, platelets have the capacity to undergo programmed cell death (Table 1). This has been most clearly demonstrated with platelet apoptosis; a process that is important for clearance of effete platelets from the circulation. 1,11 Many of the features of apoptosis (membrane fragmentation, cytoskeletal disruption, microvesiculation, caspase activation and phosphatidylserine [PS] exposure) are observed during prolonged platelet storage ex vivo and during the conversion of activated platelets to a procoagulant state, raising the possibility that apoptosis may also regulate platelet function. However, recent studies have demonstrated that the m...

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Periods without agitation diminish platelet mitochondrial function during storage

Cited by 42 publications

References 37 publications

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-κB Activation

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-κB Activation

Resveratrol Rescues Kidney Mitochondrial Function Following Hemorrhagic Shock

Procoagulant platelets: are they necrotic?

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Periods without agitation diminish platelet mitochondrial function during storage

Cited by 42 publications

References 37 publications

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-&#954;B Activation

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-&#954;B Activation

Resveratrol Rescues Kidney Mitochondrial Function Following Hemorrhagic Shock

Procoagulant platelets: are they necrotic?

Contact Info

Product

Resources

About

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-κB Activation

Treatment of Platelet Concentrates with the Mirasol Pathogen Inactivation System Modulates Platelet Oxidative Stress and NF-κB Activation