Platelet populations and priming in hematological diseases
In healthy subjects and patients with hematological diseases, platelet populations can be distinguished with different response spectra in hemostatic and vascular processes. These populations partly overlap, and are less distinct than those of leukocytes. The platelet heterogeneity is linked to stru...
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| Published in | Blood reviews Vol. 31; no. 6; pp. 389 - 399 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.11.2017
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0268-960X 1532-1681 1532-1681 |
| DOI | 10.1016/j.blre.2017.07.004 |
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| Abstract | In healthy subjects and patients with hematological diseases, platelet populations can be distinguished with different response spectra in hemostatic and vascular processes. These populations partly overlap, and are less distinct than those of leukocytes. The platelet heterogeneity is linked to structural properties, and is enforced by inequalities in the environment. Contributing factors are variability between megakaryocytes, platelet ageing, and positive or negative priming of platelets during their time in circulation. Within a hemostatic plug or thrombus, platelet heterogeneity is enhanced by unequal exposure to agonists, with populations of contracted platelets in the thrombus core, discoid platelets at the thrombus surface, patches of ballooned and procoagulant platelets forming thrombin, and coated platelets binding fibrin. Several pathophysiological hematological conditions can positively or negatively prime the responsiveness of platelet populations. As a consequence, in vivo and in vitro markers of platelet activation can differ in thrombotic and hematological disorders. |
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| AbstractList | In healthy subjects and patients with hematological diseases, platelet populations can be distinguished with different response spectra in hemostatic and vascular processes. These populations partly overlap, and are less distinct than those of leukocytes. The platelet heterogeneity is linked to structural properties, and is enforced by inequalities in the environment. Contributing factors are variability between megakaryocytes, platelet ageing, and positive or negative priming of platelets during their time in circulation. Within a hemostatic plug or thrombus, platelet heterogeneity is enhanced by unequal exposure to agonists, with populations of contracted platelets in the thrombus core, discoid platelets at the thrombus surface, patches of ballooned and procoagulant platelets forming thrombin, and coated platelets binding fibrin. Several pathophysiological hematological conditions can positively or negatively prime the responsiveness of platelet populations. As a consequence, in vivo and in vitro markers of platelet activation can differ in thrombotic and hematological disorders.In healthy subjects and patients with hematological diseases, platelet populations can be distinguished with different response spectra in hemostatic and vascular processes. These populations partly overlap, and are less distinct than those of leukocytes. The platelet heterogeneity is linked to structural properties, and is enforced by inequalities in the environment. Contributing factors are variability between megakaryocytes, platelet ageing, and positive or negative priming of platelets during their time in circulation. Within a hemostatic plug or thrombus, platelet heterogeneity is enhanced by unequal exposure to agonists, with populations of contracted platelets in the thrombus core, discoid platelets at the thrombus surface, patches of ballooned and procoagulant platelets forming thrombin, and coated platelets binding fibrin. Several pathophysiological hematological conditions can positively or negatively prime the responsiveness of platelet populations. As a consequence, in vivo and in vitro markers of platelet activation can differ in thrombotic and hematological disorders. In healthy subjects and patients with hematological diseases, platelet populations can be distinguished with different response spectra in hemostatic and vascular processes. These populations partly overlap, and are less distinct than those of leukocytes. The platelet heterogeneity is linked to structural properties, and is enforced by inequalities in the environment. Contributing factors are variability between megakaryocytes, platelet ageing, and positive or negative priming of platelets during their time in circulation. Within a hemostatic plug or thrombus, platelet heterogeneity is enhanced by unequal exposure to agonists, with populations of contracted platelets in the thrombus core, discoid platelets at the thrombus surface, patches of ballooned and procoagulant platelets forming thrombin, and coated platelets binding fibrin. Several pathophysiological hematological conditions can positively or negatively prime the responsiveness of platelet populations. As a consequence, in vivo and in vitro markers of platelet activation can differ in thrombotic and hematological disorders. |
| Author | ten Cate, Hugo Heemskerk, Johan W.M. van der Meijden, Paola E.J. Baaten, Constance C.F.M.J. |
| Author_xml | – sequence: 1 givenname: Constance C.F.M.J. surname: Baaten fullname: Baaten, Constance C.F.M.J. email: c.baaten@maastrichtuniversity.nl organization: Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands – sequence: 2 givenname: Hugo surname: ten Cate fullname: ten Cate, Hugo email: h.tencate@maastrichtuniversity.nl organization: Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands – sequence: 3 givenname: Paola E.J. surname: van der Meijden fullname: van der Meijden, Paola E.J. email: p.vandermeijden@maastrichtuniversity.nl organization: Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands – sequence: 4 givenname: Johan W.M. surname: Heemskerk fullname: Heemskerk, Johan W.M. email: jwm.heemskerk@maastrichtuniversity.nl organization: Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28756877$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Activation markers Animals Apoptosis Blood Coagulation Blood Platelets - pathology Cellular Senescence Hematologic Diseases - blood Hematologic Diseases - pathology Hemorrhage - blood Hemorrhage - pathology Humans Megakaryocytes - pathology Platelet Activation Platelet heterogeneity Positive priming Thrombosis - blood Thrombosis - pathology Thrombus |
| Title | Platelet populations and priming in hematological diseases |
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