Functional morphological alterations of human blood platelets induced by oxidized low density lipoprotein

Zhao, Bin; Dierichs, R.; Liu, B.; Holling-Rauβ, M.

doi:10.1016/0049-3848(94)90117-1

Cited by 27 publications

(17 citation statements)

References 29 publications

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“…Preparation of Ox-LDL has been reported previously [ 2 ] . Endothelial cells from bovine aorta were cultured in DMEM containing 10% FCS at 37°C in a humidified atmosphere of 5% CO, as described [I 11.…”

Section: Methodsmentioning

confidence: 99%

Endothelial cells injured by oxidized low density lipoprotein

et al. 1995

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Cultured endothelial cells from bovine aorta were exposed to oxidized low density lipoprotein and examined by electron microscopy. The endothelial cells contracted slightly and the intercellular junctions became unclear. Some osmiophilic material increased in the cytoplasm. The oxidized low density lipoprotein appears to injure endothelial cells and thereby plays a causative role in atherogenesis and thrombogenesis.

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Section: Methodsmentioning

confidence: 99%

Endothelial cells injured by oxidized low density lipoprotein

et al. 1995

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“…Oxidized LDL could also stimulate endothelial cells and increase the binding of monocytes to activated endothelial cells [9][10]. Oxidized LDL may cause significant inflammatory responses and induce physiological and biochemical disorders in endothelial cells, smooth muscle cells and blood platelets [3,[10][11][12][13][14]. It has been reported recently that circulating oxidized LDL may significantly delay endothelial wound healing [15].…”

Section: Introductionmentioning

confidence: 99%

Oxidized low‐density lipoprotein increases endothelial intracellular calcium and alters cytoskeletal f‐actin distribution

Zhao

Ehringer

Dierichs

et al. 1997

Eur J Clin Investigation

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Central to the pathogenesis of atherosclerosis is an abnormally functioning endothelium and a consequent loss of vascular integrity. These abnormalities may be induced by haemodynamic factors, biochemical substances, and also by oxidatively modified low-density lipoprotein (LDL). To understand the mechanism by which oxidized LDL causes endothelial dysfunction, human umbilical vein endothelial cells (HUVECs) were loaded with FURA-2, and intracellular calcium mobilization was studied in acute (seconds after LDL was injected) or chronic (24 h after LDL was injected) preparations. Our results demonstrate that 100 microg mL(-1) oxidized LDL increases HUVEC intracellular calcium. In contrast, native LDL at this same concentration had no effect. In addition, chronic exposure (24 h) of HUVECs to oxidized LDL significantly increases HUVEC intracellular calcium. Fluorescent photomicrographs of HUVECs stained with BODIPY-phalloidin f-actin indicates that oxidized LDL causes a reorganization of microfilaments. The results of this study demonstrate that the mechanism by which oxidized LDL causes a loss of vascular integrity could be through activation of endothelial cells to increase cytosolic calcium, which alters the endothelial barrier by reorganizing the cytoskeleton.

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“…In addition, some reports suggested that OxLDL might also affect platelet functions (10,11). OxLDL induces morphological changes, increased adhesiveness, and degranulation in platelets (12)(13)(14).…”

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confidence: 98%