ABO Blood Group Antigens on Human Plasma von Willebrand Factor After ABO-Mismatched Bone Marrow Transplantation

Blood ◽  
1999 ◽  
Vol 94 (8) ◽  
pp. 2895-2900 ◽  
Author(s):  
Taei Matsui ◽  
Taketo Shimoyama ◽  
Masanori Matsumoto ◽  
Yoshihiro Fujimura ◽  
Yoshinobu Takemoto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Stem Cell ◽  
Bone Marrow Transplantation ◽  
Stem Cell Transplantation ◽  
Blood Group ◽  
Abo Blood Group ◽  
Blood Group Antigens ◽  
Von Willebrand ◽  
Willebrand Factor

von Willebrand factor (vWF) is synthesized exclusively by endothelial cells and megakaryocytes, and stored in the intracellular granules or constitutively secreted into plasma. ABO blood group antigens are covalently associated with asparagine-linked sugar chains of plasma vWF. The effect of ABO-mismatched bone marrow transplantation (BMT) or blood stem cell transplantation (BSCT) on the expression of ABO blood group antigens on the vWF was examined to obtain information on the origin of these antigens. In ABO-mismatched (HLA-matched) groups, 8 cases of BMT and 4 cases of BSCT were examined. In all cases, the ABO blood groups on red blood cells were gradually converted to the donor’s type within 80 to 90 days after the transplantation. The blood group antigens on the vWF were consistent with the recipient’s blood group for the period monitored by enzyme-linked immunosorbent assay (ELISA). When vWF was isolated from normal platelets and examined for the blood group antigens using ELISA or immunoblotting, it showed few antigens. However, vWF extracted from veins expressed blood group antigens. These findings indicate that platelet (megakaryocyte)-derived vWF does not contain blood group antigens and that these antigens may be specifically associated with vWF synthesized in endothelial cells and secreted into plasma. Furthermore, it is possible that the persistence of the recipient’s blood group antigens on plasma glycoproteins such as vWF, independent of the donor-derived erythrocytes, after ABO-mismatched stem cell transplantation, may influence the immunological system in the production of anti-blood group antibodies resulting in the establishment of immunological tolerance in the recipient plasma.

scholarly journals ABO blood group is a determinant of von Willebrand factor protein levels in human pulmonary endothelial cells

2019 ◽  
Vol 73 (6) ◽  
pp. 347-349 ◽  
Author(s):  
Glenn P Murray ◽  
Steven R Post ◽  
Ginell R Post
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Blood Group ◽  
Von Willebrand Factor ◽  
Blood Type ◽  
Abo Blood Group ◽  
Blood Group Antigens ◽  
Protein Levels ◽  
Von Willebrand ◽  
Willebrand Factor

ABO blood group antigens are expressed on von Willebrand factor (VWF) and glycosylation patterns influence circulating VWF levels. The aim of this study was to examine the effect of ABO blood type on tissue-associated VWF protein levels. We selected 35 formalin-fixed paraffin-embedded pulmonary tissue blocks obtained at autopsy from decedents who died from pulmonary embolism with known ABO blood groups (O, A, B and AB phenotypes), prepared tissue microarrays (TMAs) and stained TMAs with antibodies to VWF and platelet/endothelial cell adhesion marker-1 (PECAM-1) as a marker of endothelial cells. A pixel count scoring algorithm was used to quantify VWF and PECAM-1 staining intensity in pulmonary arterioles in digitised images. Compared with type O, non-O individuals have a significantly higher amount of endothelial cell-associated VWF protein expression. VWF protein levels associated with pulmonary vascular endothelial cells is influenced by ABO antigenic determinants.

Heterogeneous Detection of A-antigen on von Willebrand Factor Derived from Platelets, Endothelial Cells and Plasma

2002 ◽  
Vol 87 (06) ◽  
pp. 990-996 ◽  
Author(s):  
Peter Collins ◽  
Derrick Bowen ◽  
Simon Brown
Keyword(s):  
Endothelial Cells ◽  
Blood Group ◽  
Von Willebrand Factor ◽  
Saphenous Vein ◽  
Umbilical Vein ◽  
Abo Blood Group ◽  
Blood Group Antigens ◽  
Exact Function ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryThe exact function of the carbohydrate component of von Willebrand factor (VWF) is unknown. ABO blood group antigens are present as integral structures on the oligosaccharide side chains and it has long been recognised that ABO blood group is a determinant of VWF levels. The mechanism for this is not known. Using a monoclonal antibody against the A-antigen, we investigated the presence of this antigen on VWF from plasma, platelets, human umbilical vein endothelial cells (HUVEC) and saphenous vein endothelial cells. Initial studies on plasma VWF revealed that 23.5% of samples appeared to be negative for the A-antigen. This was shown to correlate with the A2 subtype of the A-antigen (p <0.01). Analysis of intracellular VWF from saphenous vein endothelial cells revealed low levels of A-antigen to be present in comparison to the corresponding plasma VWF. In contrast, VWF from platelets and HUVEC gave no detectable A-antigen. However, within 1 h of administration of DDAVP to type 1 VWD patients, there was a >2-fold increase in the A-antigen/VWF:Ag ratio for VWF in the plasma. In vitro experiments with serum N-acetlygalactosaminyltransferase failed to demonstrate any addition of A-antigen to platelet or HUVEC VWF. These data are consistent with heterogeneity in the content of A-antigen on VWF from different physiological compartments. Also, they are consistent with either a change in the A-antigen content of VWF after release from the intracellular compartment or a difference in the intracellular addition of A-antigen to VWF by endothelium from different vascular beds.

scholarly journals What would Karl Landsteiner do? The ABO blood group and stem cell transplantation

2005 ◽  
Vol 36 (9) ◽  
pp. 747-755 ◽  
Author(s):  
J M Heal ◽  
J L Liesveld ◽  
G L Phillips ◽  
N Blumberg
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Cell Transplantation ◽  
Blood Group ◽  
Abo Blood Group

Whole Blood Tissue Factor Procoagulant Activity Remains Detectable during Severe Aplasia following Bone Marrow and Peripheral Blood Stem Cell Transplantation

2001 ◽  
Vol 85 (02) ◽  
pp. 250-255 ◽  
Author(s):  
Muhit Ozcan ◽  
Colleen Morton ◽  
Anna Solovey ◽  
Luke Dandelet ◽  
Ronald Bach ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Endothelial Cells ◽  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Tissue Factor ◽  
Cell Transplantation ◽  
Whole Blood ◽  
Peripheral Blood ◽  
Peripheral Blood Stem Cell ◽  
Blood Stem Cell Transplantation

SummaryUsing a novel whole blood assay, we recently demonstrated that tissue factor procoagulant activity (TF PCA) is present in normal individuals. Preliminary experiments suggested that this activity is localized in the mononuclear cell fraction. Postulating that whole blood TF PCA would therefore be undetectable when monocytes and neutrophils are absent from peripheral blood, we assayed TF PCA during the peri-transplant period in 15 consecutive patients undergoing allogeneic (n = 12) or autologous (n = 3) bone marrow transplantation (BMT) or peripheral blood stem cell transplantation (PBSCT). Baseline (pre-transplant) mean TF PCA was higher in patients compared to normal controls (P <0.005). Unexpectedly, although TF PCA during the period of profound aplasia was significantly reduced compared to baseline (p <0.05), fully 55% of the initial activity remained detectable. During the engraftment phase, TF PCA returned to pre-transplant levels, with a linear correlation between monocyte counts and TF PCA (r = 0.63). In contrast to normal whole blood, incubation of aplastic samples with E. Coli lipopolysaccharide ex vivo failed to induce TF PCA. Throughout the period of study – but especially during the aplastic phase – the absolute number of circulating endothelial cells (CECs) that were TF antigen-positive was increased compared to normals (P <0.001). However, removal of these cells from whole blood samples failed to significantly diminish total TF PCA indicating that CECs alone could not account for the detectable TF PCA during aplasia. We conclude that neither circulating mature myelo-monocytic cells nor endothelial cells can account for all the functionally intact TF in peripheral blood. Further studies are needed to identify the other source(s) of TF PCA.

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