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Original ArticleOpen Access
Modification of Platelet Shape Change Parameter by Oxidized Lipoprotein from β-thalassemia/Hemoglobin E
Sutipornpalangkul W 
,
Unchern S ,
Sanvarinda Y ,
Chantharaksri U ,
Fucharoen S
,
Unchern S ,
Sanvarinda Y ,
Chantharaksri U ,
Fucharoen S Background: β-thalassemia/Hemoglobin E (β-thal/Hb E) is a congenital hemolytic anemia that is prevalent
in Thailand. Pulmonary arterial occlusion is the cause of morbidity and mortality in these patients. Abnormality
of platelets has been implicated as pathogenesis of this condition. However, the blood-borne factors that
induce platelet activation are not identified. Recently, oxidized low-density lipoproteins (ox-LDLs) had been
identified in thalassemic blood.
Objective: Identify whether oxidized LDL is the blood bone factor that induce platelet activation in β-thal/Hb
E patients.
Material and Method: Platelet activation was measured by monitoring platelet shape change parameter
using plasma-free human platelets. The shape change parameter was monitored following exposure to normal
LDL, oxidized LDL, and thalassemic LDL.
Results: Oxidized LDL, but not the native LDL and thalassemic LDL, showed platelet activation activity.
Oxidation of thalassemic LDL with copper give rise to oxidized LDL with platelet activating activity. However,
less copper was needed by LDL from splenectomized β-thal/Hb E patients than those from nonsplencectomized
β-thal/Hb E patients.
Conclusion: LDL from splenectomized β-thal/Hb E patients is more susceptible for oxidation and gives rise to
oxidized-LDL that plays an important role in thrombosis event in these patients.
Keywords: Blood platelets, Cell shape, Hemoglobin E, Oxidized low density lipoprotein, Lipoproteins, LDL,
Thalassemia
in Thailand. Pulmonary arterial occlusion is the cause of morbidity and mortality in these patients. Abnormality
of platelets has been implicated as pathogenesis of this condition. However, the blood-borne factors that
induce platelet activation are not identified. Recently, oxidized low-density lipoproteins (ox-LDLs) had been
identified in thalassemic blood.
Objective: Identify whether oxidized LDL is the blood bone factor that induce platelet activation in β-thal/Hb
E patients.
Material and Method: Platelet activation was measured by monitoring platelet shape change parameter
using plasma-free human platelets. The shape change parameter was monitored following exposure to normal
LDL, oxidized LDL, and thalassemic LDL.
Results: Oxidized LDL, but not the native LDL and thalassemic LDL, showed platelet activation activity.
Oxidation of thalassemic LDL with copper give rise to oxidized LDL with platelet activating activity. However,
less copper was needed by LDL from splenectomized β-thal/Hb E patients than those from nonsplencectomized
β-thal/Hb E patients.
Conclusion: LDL from splenectomized β-thal/Hb E patients is more susceptible for oxidation and gives rise to
oxidized-LDL that plays an important role in thrombosis event in these patients.
Keywords: Blood platelets, Cell shape, Hemoglobin E, Oxidized low density lipoprotein, Lipoproteins, LDL,
Thalassemia
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