In vitro function and phagocytosis of galactosylated platelet concentrates after long‐term refrigeration

Babić, Aleksandar; Josefsson, Emma C.; Bergmeier, Wolfgang; Wagner, Denisa D.; Kaufman, Richard M.; Silberstein, Leslie E.; Stossel, Thomas P.; Hartwig, John H.; Hoffmeister, Karin M.

doi:10.1111/j.1537-2995.2007.01134.x

Cited by 54 publications

(120 citation statements)

References 20 publications

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“…11,30 We observed some increase in P-selectin and phosphatidyl serine expression on murine platelets after 48 hours of cold storage. In contrast, P-selectin and phosphatidyl serine expression on the cold-stored human platelets were similar to those of platelets stored at RT (Table 3).…”

Section: Discussionmentioning

confidence: 78%

“…10 Platelet aggregation and agglutination experiments were performed with a PLT aggregation profiler (Model PAP-; Bio/Data, Horsham, PA). Platelets were washed and resuspended as previously described 11 and activated by adding 0.1 U to 1 U thrombin (Sigma-Aldrich, St Louis, MO) per mL; platelet-rich plasma (PRP) was mixed with platelet-poor plasma (PPP) in the ratio 1:1 and was then activated through the addition of 1.5 mg/mL ristocetin (Sigma-Aldrich) for 3 minutes at 37°C under constant stirring (1000 rpm). Resuspension buffer for washed PLTs and PPP for PRP were set as maximum of light transmission.…”

Section: Human Platelet Studiesmentioning

confidence: 99%

“…This galactosylation process inhibited the in vitro phagocytosis of human galactosylated platelets by THP-1 cells, suggesting that galactosylated platelets stored at 4°C might circulate when transfused into humans. 11 Reported here are the results of a phase 1 clinical trial in which autologous apheresis platelets obtained from healthy volunteers were stored for 48 hours using different storage conditions before reinfusion: galactosylated platelets stored at 4°C, nongalactosylated platelets stored at 4°C, or nongalactosylated platelets stored at room temperature (22°C). In addition, similar platelet storage studies were performed using murine platelets in a mouse model.…”

Section: Introductionmentioning

confidence: 99%

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Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Wandall

Hoffmeister

Sørensen

et al. 2008

Blood

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Cold storage of platelets for transfusion is desirable to extend platelet storage times and to prevent bacterial growth. However, the rapid clearance of coldstored platelets prevents their use. A novel method for preventing the rapid clearance of cold-stored platelets has previously been developed in a murine model. Cold storage induces the clustering and recognition of exposed ␤-Nacetylglucosamine (␤GlcNAc) on platelet surfaces. Glycosylation of ␤GlcNAc residues with uridine 5-diphosphogalactose (UDP-galactose) results in the normal survival of short-term (2 h) 0°C-stored murine platelets. Based on this finding, we developed a similar glycosylation process by adding UDP-galactose to human apheresis platelets. A phase 1 clinical trial was conducted transfusing radiolabeled autologous apheresis platelets stored for 48 hours at 4°C with or without pretreatment with UDP-galactose. In contrast to the murine study, galactosylation of human platelets did not prevent the accelerated platelet clearance routinely observed after 4°C storage. We next developed a murine model of platelet storage for 48 hours at 4°C and showed that UDP-galactose treatment of murine platelets also did not prevent their rapid clearance, in agreement with the human platelet study. We conclude that different mechanisms of clearance may exist for short-and long-term cold-stored platelets. (Blood. 2008;111:3249-3256)

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Section: Discussionmentioning

confidence: 78%

Section: Human Platelet Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Wandall

Hoffmeister

Sørensen

et al. 2008

Blood

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“…[23][24][25] Unfortunately, the coldinflicted changes in GPIbα collectively defined as GPIbα clustering prevents rapid introduction into transfusion medicine. The present results describe the molecular mechanism of cold-induced GPIbα clustering.…”

Section: Discussionmentioning

confidence: 99%

Improved platelet survival after cold storage by prevention of glycoprotein Ib clustering in lipid rafts

et al. 2012

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The online version of this article has a Supplementary Appendix. BackgroundStoring platelets for transfusion at room temperature increases the risk of microbial infection and decreases platelet functionality, leading to out-date discard rates of up to 20%. Cold storage may be a better alternative, but this treatment leads to rapid platelet clearance after transfusion, initiated by changes in glycoprotein Ibα, the receptor for von Willebrand factor. Design and MethodsWe examined the change in glycoprotein Ibα distribution using Förster resonance energy transfer by time-gated fluorescence lifetime imaging microscopy. ResultsCold storage induced deglycosylation of glycoprotein Ibα ectodomain, exposing N-acetyl-Dglucosamine residues, which sequestered with GM1 gangliosides in lipid rafts. Raft-associated glycoprotein Ibα formed clusters upon binding of 14-3-3ζ adaptor proteins to its cytoplasmic tail, a process accompanied by mitochondrial injury and phosphatidyl serine exposure. Cold storage left glycoprotein Ibα surface expression unchanged and although glycoprotein V decreased, the fall did not affect glycoprotein Ibα clustering. Prevention of glycoprotein Ibα clustering by blockade of deglycosylation and 14-3-3ζ translocation increased the survival of cold-stored platelets to above the levels of platelets stored at room temperature without compromising hemostatic functions. ConclusionsWe conclude that glycoprotein Ibα translocates to lipid rafts upon cold-induced deglycosylation and forms clusters by associating with 14-3-3ζ. Interference with these steps provides a means to enable cold storage of platelet concentrates in the near future.Key words: platelets, cold storage, glycoprotein Ibα, 14-3-3ζ, lipid raft, clustering. Ibα clustering in lipid rafts. Haematologica 2012;97(12):1873-1881. doi:10.3324/haematol.2012 This is an open-access paper. Citation: Gitz E, Koekman CA, van den Heuvel DJ, Deckmyn H, Akkerman JW, Gerritsen HC and Urbanus RT. Improved platelet survival after cold storage by prevention of glycoprotein Improved platelet survival after cold storage by prevention of glycoprotein Ibα clustering in lipid rafts ABSTRACT© F e r r a t a S t o r t i F o u n d a t i o n

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“…48 Furthermore, cold storage better preserves the platelets' capacity to aggregate and secrete their granule contents upon later stimulation at 37°C. 49,50 AA depletion will reduce platelet activation during preparation of platelet concentrates, since mechanical disturbances can activate this metabolic pathway. 51 Since this process is reversible, addition of AA prior to transfusion -or when transfused platelets bind plasma AA-albumin in the circulation -will fully restore hemostatic functions.…”

Section: Discussionmentioning

confidence: 99%

Arachidonic acid depletion extends survival of cold-stored platelets by interfering with the [glycoprotein Ib - 14-3-3 ] association

Wal

Gitz

et al. 2012

Haematologica

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In vitro function and phagocytosis of galactosylated platelet concentrates after long‐term refrigeration

Abstract: It is shown that refrigerated human PLTs retain in vitro function better than RT PLTs during storage and demonstrate that galactosylation prevents recognition of stored refrigerated PLTs by macrophages in vitro.

Cited by 54 publications

References 20 publications

Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets

Improved platelet survival after cold storage by prevention of glycoprotein Ib clustering in lipid rafts

Arachidonic acid depletion extends survival of cold-stored platelets by interfering with the [glycoprotein Ib - 14-3-3 ] association

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