Early increase in DcR2 expression and late activation of caspases in the platelet storage lesion

Plenchette, Stéphanie; Moutet, Monique; Benguella, M; N'Gondara, JP; Guigner, F; Coffe, C; Corcos, Laurent; Bettaieb, Ali; Solary, Éric

doi:10.1038/sj.leu.2402231

Cited by 51 publications

(42 citation statements)

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“…[42][43][44][45][46][47] The possibility of stored platelets undergoing secondary necrosis may partly explain the inability of apoptosis inhibitors to maintain the viability of stored platelet concentrates. 48,49 Would agents that preserve mitochondrial function improve the viability of stored platelets? Much of the current effort into improving the viability of stored platelet concentrates has focused on reducing platelet activation, maintaining pH, buffering lactate production and enhancing gas exchange.…”

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

confidence: 99%

Procoagulant platelets: are they necrotic?

Jackson

Schoenwaelder

2010

Blood

143

141

View full text Add to dashboard Cite

show abstract

“…Also, it has been reported that melanoma cells are frequently resistant at the time of surgical excision, but regain sensitivity in cell culture (Nguyen et al, 2001). A similar effect has been demonstrated in platelets that have been stored for transfusion, where there is an early increase in the expression of DcR2, but this increase in expression is not enough to protect platelets from lesion, caused by apoptosis and caspase activation of these cells (Plenchette et al, 2001). It is therefore important to develop an understanding of the factors that lead to sensitivity or resistance of tumour cells to Apo2L/TRAIL.…”

Section: Discussionmentioning

confidence: 69%

Progressive resistance of BTK-143 osteosarcoma cells to Apo2L/TRAIL-induced apoptosis is mediated by acquisition of DcR2/TRAIL-R4 expression: resensitisation with chemotherapy

et al. 2003

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“…Storage for longer periods of time leads to impaired platelet function, known as platelet storage lesion (PSL) [20]. Some of the morphological and biochemical aspects of the PSL have been compared to apoptotic events [21,22] and it is interesting to note that glucose deprivation is known to lead to apoptosis [23,24]. It has been shown that calpain is activated during platelet storage and that several signalling molecules translocate to the cytoskeleton after stress induced calpain activation indicating a critical role of the cytoskeleton in platelet ageing [14].…”

Section: Discussionmentioning

confidence: 99%