Buffy‐coat platelet variables and metabolism during storage in additive solutions or plasma

Zhang, Jerry G.; Carter, Cedric J.; Culibrk, Brankica; Devine, Dana V.; Levin, E.J.; Scammell, Kenneth; Weiss, Sandra; Gyöngyössy‐Issa, Maria I.C.

doi:10.1111/j.1537-2995.2008.01645.x

Cited by 63 publications

(66 citation statements)

References 47 publications

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“…P-selectin increased with time as shown by us and others [6,13,31]. PS exposure increased only minimally during the normal shelf-life of PCs but by day 12, the exposure had increased significantly.…”

Section: Discussionmentioning

confidence: 73%

Platelet adhesion changes during storage studied with a novel method using flow cytometry and protein-coated beads

et al. 2014

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The aim of the present study was to set up and evaluate a novel method for studies of platelet adhesion and activation in blood and platelet suspensions such as platelet concentrate (PC) samples using protein-coated polystyrene beads and flow cytometry. To demonstrate its usefulness, we studied PCs during storage. PCs were prepared by apheresis technique (N = 7).Metabolic variables and platelet function was measured on day 1, 5, 7 and 12 of storage.Spontaneous and TRAP-6-induced adhesion to fibrinogen-and collagen-coated beads was analysed by flow cytometry. P-selectin and phosphatidyl serine (PS) expression was assessed on platelets bound to beads as well as on non-adherent platelets. Platelet adhesion to fibrinogen beads had increased by day 12 and adhesion to collagen beads at day 7 of storage (p < 0.05). TRAP-6 stimulation significantly increased the platelet adhesion to fibrinogen beads (p < 0.05) as well as the P-selectin and PS exposure on platelets bound to beads (p < 0.01) during the first 7 days of storage, but by day 12, significant changes were no longer induced by TRAP-6 stimulation.We demonstrate that our adhesion assay using protein-coated polystyrene beads can be used to assess the adhesion properties of platelets during storage without the addition of red blood cells. Therefore it may offer a useful tool for future studies of platelet adhesive capacity in transfusion medicine and other settings.3

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Section: Discussionmentioning

confidence: 73%

Platelet adhesion changes during storage studied with a novel method using flow cytometry and protein-coated beads

et al. 2014

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“…It is well known that various components of serum and plasma promote spreading of adherent cells on tissue-culture plastic (43,44). TSOL is a chemical formulation (sodium citrate-acetate-chloride) and does not contain any of the biochemical compounds present in plasma (45); the absence of these compounds may contribute to the decreased spreading observed when the cells were treated with the plasma-free additive, TSOL.…”

Section: Discussionmentioning

confidence: 99%

Comparison of human platelet lysate alternatives using expired and freshly isolated platelet concentrates for adipose-derived stromal cell expansion

2018

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Pooled human platelet lysate (pHPL) has been used to expand adipose-derived stromal cells (ASCs) and can be formulated using fresh or expired buffy coats (BCs) which are then resuspended in either plasma or an additive solution. Not much is known about the effects that expired products and additive solutions have on ASC expansion, and the need for quality control and release criteria has been expressed. This pilot study compared proliferation, cell size, morphology and immunophenotype of ASCs expanded in the different pHPL alternatives versus foetal bovine serum (FBS). Quality control criteria were assessed prior to and during the manufacture of the pHPL alternatives. ASCs were then expanded in 1%, 2.5%, 5% or 10% of the different pHPL alternatives or in 10% FBS. Cell size, morphology, cell number and immunophenotype were measured using microscopy and flow cytometry. The majority of the pHPL alternatives were within the recommended ranges for the quality control criteria. ASCs expanded in the pHPL alternatives were smaller in size, displayed a tighter spindle-shaped morphology, increased cell growth and had a similar immunophenotype (with the exception of CD34 and CD36) when compared to ASCs expanded in FBS. Here we report on the effects that expired BC products and additive solutions have on ASC expansion. When taken together, our findings indicate that all of the pHPL alternatives can be considered to be suitable replacements for FBS for ASC expansion, and that expired BC products can be used as an alternative to fresh BC products. KeywordsAdditive solution, adipose-derived stromal cells, expired buffy coats, foetal bovine serum, pooled human platelet lysate History

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“…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. 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.…”

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

confidence: 99%

“…Consistent with this, metabolic disturbance has been reported to play a role in the loss of platelet viability during PSL. [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?…”

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

confidence: 99%

Procoagulant platelets: are they necrotic?

Jackson

Schoenwaelder

2010

Blood

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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Buffy‐coat platelet variables and metabolism during storage in additive solutions or plasma

Abstract: Newer PASs, for example, SSP+ and Composol, can maintain PLT integrity and moderate metabolism similarly to plasma but offer consistently lower PLT recoveries and limited osmotic balance.

Cited by 63 publications

References 47 publications

Platelet adhesion changes during storage studied with a novel method using flow cytometry and protein-coated beads

Platelet adhesion changes during storage studied with a novel method using flow cytometry and protein-coated beads

Comparison of human platelet lysate alternatives using expired and freshly isolated platelet concentrates for adipose-derived stromal cell expansion

Procoagulant platelets: are they necrotic?

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