Advanced search
1 file | 338.53 KB

The contribution of von Willebrand factor-GPIbα interactions to persistent aggregate formation in apheresis platelet concentrates

(2016) VOX SANGUINIS. 110(4). p.344-351
Author
Organization
Abstract
BACKGROUND AND OBJECTIVES: Apheresis platelet concentrates sometimes contain persistent aggregates (PA). Because apheresis involves extracorporeal circulation, we hypothesized that interactions between GPIbα and von Willebrand factor (VWF) underlie their origin. MATERIALS AND METHODS: Platelets in donations with PA were compared to aggregate-free (AF) controls. Flow cytometry was used to determine platelet bound VWF. Degranulation was measured using P-selectin expression in flow cytometry and cytokine release using immunosorbent assays. Platelet adhesion to VWF was assessed in hydrodynamic flow and real-time video microscopy. RESULTS: Platelets in PA concentrates had significantly more (P = 0·009, n ≥ 8) bound VWF compared to AF platelets, but differences in VWF concentration, VWF collagen binding, activated VWF or GPIbα expression were not found. Degranulation was higher (P = 0·030, n = 7) in PA than AF concentrates on day 1 of storage, but adhesion to immobilized VWF under hydrodynamic flow conditions was normal at that moment. On day 6, however, significantly less VWF adhesion (P = 0·009, n ≥ 6) was found for PA platelets compared to AF, indicating accelerated storage lesion in PA products. In a model that mimicks PA formation by chemically induced binding of VWF to platelets, we found that degranulation, phosphatidylserine expression and metabolism did not differ with paired controls at any time during subsequent storage. CONCLUSION: Accelerated storage lesion is found in concentrates with PA, but this cannot be explained solely by increased platelet bound VWF following apheresis. Therefore, additional stressors are probably responsible for the increases observed in platelet degranulation and storage lesion in products with PA.
Keywords
von Willebrand factor, storage lesion, platelets, aggregates, apheresis, IX-MEDIATED ACTIVATION, GLYCOPROTEIN IB-ALPHA, INTEGRIN ALPHA(IIB)BETA(3), VONWILLEBRAND-FACTOR, DISEASE, BINDING, ADHESION, COMPLEX, RISK, 2B

Downloads

  • 20 The Contribution of Von Willebrand factor-GpIba interactions to persistent aggregate formation in apheresis platelet concentrates.pdf
    • full text
    • |
    • open access
    • |
    • PDF
    • |
    • 338.53 KB

Citation

Please use this url to cite or link to this publication:

Chicago
Feys, Hendrik, Britt Van Aelst, Rosalie Devloo, Philippe Vandekerckhove, and Veerle Compernolle. 2016. “The Contribution of Von Willebrand factor-GPIbα Interactions to Persistent Aggregate Formation in Apheresis Platelet Concentrates.” Vox Sanguinis 110 (4): 344–351.
APA
Feys, Hendrik, Van Aelst, B., Devloo, R., Vandekerckhove, P., & Compernolle, V. (2016). The contribution of von Willebrand factor-GPIbα interactions to persistent aggregate formation in apheresis platelet concentrates. VOX SANGUINIS, 110(4), 344–351.
Vancouver
1.
Feys H, Van Aelst B, Devloo R, Vandekerckhove P, Compernolle V. The contribution of von Willebrand factor-GPIbα interactions to persistent aggregate formation in apheresis platelet concentrates. VOX SANGUINIS. 2016;110(4):344–51.
MLA
Feys, Hendrik, Britt Van Aelst, Rosalie Devloo, et al. “The Contribution of Von Willebrand factor-GPIbα Interactions to Persistent Aggregate Formation in Apheresis Platelet Concentrates.” VOX SANGUINIS 110.4 (2016): 344–351. Print.
@article{7054826,
  abstract     = {BACKGROUND AND OBJECTIVES: Apheresis platelet concentrates sometimes contain persistent aggregates (PA). Because apheresis involves extracorporeal circulation, we hypothesized that interactions between GPIb\ensuremath{\alpha} and von Willebrand factor (VWF) underlie their origin.
MATERIALS AND METHODS: Platelets in donations with PA were compared to aggregate-free (AF) controls. Flow cytometry was used to determine platelet bound VWF. Degranulation was measured using P-selectin expression in flow cytometry and cytokine release using immunosorbent assays. Platelet adhesion to VWF was assessed in hydrodynamic flow and real-time video microscopy.
RESULTS: Platelets in PA concentrates had significantly more (P = 0{\textperiodcentered}009, n \ensuremath{\geq} 8) bound VWF compared to AF platelets, but differences in VWF concentration, VWF collagen binding, activated VWF or GPIb\ensuremath{\alpha} expression were not found. Degranulation was higher (P = 0{\textperiodcentered}030, n = 7) in PA than AF concentrates on day 1 of storage, but adhesion to immobilized VWF under hydrodynamic flow conditions was normal at that moment. On day 6, however, significantly less VWF adhesion (P = 0{\textperiodcentered}009, n \ensuremath{\geq} 6) was found for PA platelets compared to AF, indicating accelerated storage lesion in PA products. In a model that mimicks PA formation by chemically induced binding of VWF to platelets, we found that degranulation, phosphatidylserine expression and metabolism did not differ with paired controls at any time during subsequent storage.
CONCLUSION: Accelerated storage lesion is found in concentrates with PA, but this cannot be explained solely by increased platelet bound VWF following apheresis. Therefore, additional stressors are probably responsible for the increases observed in platelet degranulation and storage lesion in products with PA.},
  author       = {Feys, Hendrik and Van Aelst, Britt and Devloo, Rosalie and Vandekerckhove, Philippe and Compernolle, Veerle},
  issn         = {0042-9007},
  journal      = {VOX SANGUINIS},
  language     = {eng},
  number       = {4},
  pages        = {344--351},
  title        = {The contribution of von Willebrand factor-GPIb\ensuremath{\alpha} interactions to persistent aggregate formation in apheresis platelet concentrates},
  url          = {http://dx.doi.org/10.1111/vox.12365},
  volume       = {110},
  year         = {2016},
}

Altmetric
View in Altmetric
Web of Science
Times cited: