摘要
Elevated plasma levels of high density lipoprotein (HDL) are recognized as having a beneficial influence on the progression of atherosclerosis. As platelets are closely involved in atherosclerogenesis, it is difficult to evaluate if the protective effect of HDL is associated with its ability to affect platelet structure and function. Previous studies give conflicting reports concerning the HDL platelet interaction. In our in vitro experiments, washed human blood platelets were preincubated with HDL (100 800 μg/ml) and then stimulated by serotonin (5 Hydroxytryptamine, 1 5 μM), a potent agonist and mediator in the process of atherosclerosis. Aggregatory studies and electron microscopy revealed that HDL could not prevent morphological alterations of blood platelets treated with serotonin. Furthermore, high dosages of HDL led to platelet activation. These findings indicate that HDL may not inhibit agonist induced platelet activation. As HDL is a heterogeneous group of different subclasses with opposite effects on platelet function, it Platelet Research Unit, Institute of Anatomy, University of Münster, Germany (Pfennig O and Dierichs R) Institute of Physiology, Ruhr University Bochum, Bochum, Germany (Liu B) can be concluded that HDL platelet interaction reflects relative concentrations of the particular sample. Our findings suggest that the protective influence of HDL may not be associated with decreased platelet function. Apoprotein E rich subclasses of HDL (HDL 2), particularly HDL enriched apoprotein E (HDL E), inhibit agonist induced platelet activation. In order to enlighten the role of apo E in this process, platelets in suspensions were preincubated with purified apoprotein E (50 400 μg/ml) and then stimulated by serotonin (5 μM). Apoprotein E of 300 μg/ml prevented morphological alterations of blood platelets and suppressed serotonin induced activation. Lower concentrated apoprotein E showed no clear effects. There is evidence that apoprotein E is an important factor in the prevention of atherosclerosis, by enhancing the reversed cholesterol transport to the liver and modifiing the functional status of different cell types such as macrophages and smooth muscle cells. Because results showed effects of apo R on platelet activation, we suggest that apoprotein E may be a principal factor when platelet aggregability is suppressed by HDL subclasses or liposomes and that the antiatherogenic potency of apo E correlates with this process.
Elevated plasma levels of high density lipoprotein (HDL) are recognized as having a beneficial influence on the progression of atherosclerosis. As platelets are closely involved in atherosclerogenesis, it is difficult to evaluate if the protective effect of HDL is associated with its ability to affect platelet structure and function. Previous studies give conflicting reports concerning the HDL platelet interaction. In our in vitro experiments, washed human blood platelets were preincubated with HDL (100 800 μg/ml) and then stimulated by serotonin (5 Hydroxytryptamine, 1 5 μM), a potent agonist and mediator in the process of atherosclerosis. Aggregatory studies and electron microscopy revealed that HDL could not prevent morphological alterations of blood platelets treated with serotonin. Furthermore, high dosages of HDL led to platelet activation. These findings indicate that HDL may not inhibit agonist induced platelet activation. As HDL is a heterogeneous group of different subclasses with opposite effects on platelet function, it Platelet Research Unit, Institute of Anatomy, University of Münster, Germany (Pfennig O and Dierichs R) Institute of Physiology, Ruhr University Bochum, Bochum, Germany (Liu B) can be concluded that HDL platelet interaction reflects relative concentrations of the particular sample. Our findings suggest that the protective influence of HDL may not be associated with decreased platelet function. Apoprotein E rich subclasses of HDL (HDL 2), particularly HDL enriched apoprotein E (HDL E), inhibit agonist induced platelet activation. In order to enlighten the role of apo E in this process, platelets in suspensions were preincubated with purified apoprotein E (50 400 μg/ml) and then stimulated by serotonin (5 μM). Apoprotein E of 300 μg/ml prevented morphological alterations of blood platelets and suppressed serotonin induced activation. Lower concentrated apoprotein E showed no clear effects. There is evidence that apoprotein E is an important factor in the prevention of atherosclerosis, by enhancing the reversed cholesterol transport to the liver and modifiing the functional status of different cell types such as macrophages and smooth muscle cells. Because results showed effects of apo R on platelet activation, we suggest that apoprotein E may be a principal factor when platelet aggregability is suppressed by HDL subclasses or liposomes and that the antiatherogenic potency of apo E correlates with this process.
