Platelet activation results in a redistribution of glycoprotein IV (CD36).

Michelson, Alan D.; Wencel-Drake, June D.; Kestin, Anita S.; Barnard, Marc R.

doi:10.1161/01.atv.14.7.1193

Cited by 36 publications

(26 citation statements)

References 63 publications

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“…However, with thrombin in particular, agonist stimulation of platelets from WAS patients resulted in a defective capacity to activate, as measured by increased CD62P (P selectin, an alpha-granule protein) or CD63 (platelet lysosomal protein) expression. These proteins are normally translocated to the platelet surface with thrombin activation (McEver & Martin, 1984;Niewenhuis et al, 1987); ADP activation usually causes less translocation (Michelson et al, 1994). The reasons for the defective CD62/CD63 activation patterns in the WAS platelets are unknown, but they are consistent with the muted ability of these platelets to modulate GPIIbIIIa expression following agonist stimulation.…”

Section: Discussionmentioning

confidence: 98%

Flow cytometric analysis of platelets from childrenwith the Wiskott‐Aldrich syndrome reveals defects in platelet development, activation and structure

Semple

Siminovitch

Mody³

et al. 1997

Br J Haematol

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Summary. The pathophysiology of platelet dysfunction in the Wiskott-Aldrich immune deficiency syndrome (WAS) remains unclear. Using flow cytometry, we have characterized the functional properties of platelets from 10 children with WAS. Patients with WAS had thrombocytopenia, small platelets, increased platelet-associated IgG and reduced platelet-dense granule content. Levels of reticulated 'young' platelets were normal in the WAS patients. Although the mean numbers of platelet glycoprotein (GP) Ib, GPIIbIIIa and GPIV molecules per platelet appeared lower in WAS patients than in healthy controls, analysis of similar-sized platelets revealed the mean number of GPIb molecules per platelet to be comparable in patients and normal controls. Surface GPIIbIIIa and GPIV expression was, however, significantly lower on the WAS platelets than on normal platelets. Compared with normal platelets, WAS platelets showed a reduced ability to modulate GPIIbIIIa expression following thrombin stimulation. In addition, thrombin-and ADPinduced expression of CD62P and CD63 was defective in WAS platelets. Phallacidin staining of the WAS platelets revealed less F-actin content than in normal platelets. Together, these data suggest that the reduced platelet number and function in WAS reflects, at least in part, a defect in bone marrow production as well as an intrinsic platelet abnormality.

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Section: Discussionmentioning

confidence: 98%

Flow cytometric analysis of platelets from childrenwith the Wiskott‐Aldrich syndrome reveals defects in platelet development, activation and structure

Semple

Siminovitch

Mody³

et al. 1997

Br J Haematol

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“…When intense platelet stimulation occurs, ␣ IIb ␤ 3 and CD36 are redistributed, and surface expression increases, corresponding to the membrane exposition of the intracellular granular pool. 16,17 Two additional proteins normally absent from the platelet surface, P-selectin (GMP-140 and CD62P), abundant in ␣-granules, and CD63, a lysosomal component, are exposed on the plasma membrane after secretion of granular contents. 18,19 At day 0, normal CD36 and ␣ IIb ␤ 3 epitopes were both correlated with the platelet size.…”

Section: Discussionmentioning

confidence: 99%

High Plasma Serotonin Levels in Primary Pulmonary Hypertension

Keréveur

Crinon

Humbert

et al. 2000

ATVB

129

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Elevated plasma serotonin is associated with primary pulmonary hypertension (PPH). To test whether this elevation could be related to platelet activation, the 2 pools of blood serotonin (platelets and plasma) and plasma 5-hydroxyindoleacetic acid (5-HIAA) as well as markers of platelet activation (alpha(IIb)beta(3), CD36, P-selectin, and CD63 membrane epitopes) were measured in 16 patients with severe PPH (group 1) before and at days 10 and 40 of treatment with a continuous infusion of epoprostenol (prostacyclin). The same biological parameters were also measured in 19 healthy subjects (group 2) and in 10 patients after cardiovascular surgery with extracorporeal circulation (group 3), a condition known to profoundly activate the platelets. Twelve PPH patients showed hemodynamic and clinical improvement, 3 remained stable, and 1 had the treatment stopped because of clinical aggravation. At day 0, mean plasma serotonin (5-hydroxytryptamine [5-HT]) concentration was much higher in PPH patients than in normal subjects (34.4+/-21.2 versus 9.1+/-6.0 nmol/L, respectively; P:<0.001) and positively correlated with total pulmonary resistance. The mean platelet 5-HT content was not significantly different in PPH compared with normal individuals. Mean plasma 5-HIAA concentrations were much higher in PPH than in normal patients (162+/-57 versus 61+/-7 nmol/L, respectively; P<0.001). These parameters did not significantly change during epoprostenol treatment. There was no correlation between the changes in plasma 5-HT during treatment and clinical or hemodynamic improvement. In PPH patients, the mean platelet volume significantly decreased (ANOVA, P<0.01) during treatment. Positive correlations were evidenced between the size of platelets and the number of alpha(IIb)beta(3) and CD36 epitopes. When compared with control platelets, the number of alpha(IIb)beta(3) epitopes detected on PPH platelets at day 0 tended to be higher, but this difference did not reach a statistical significance (41 300+/-7140 for PPH patients versus 36 010+/-3930 for control subjects, P=0.069). The number of CD36 epitopes, in the range of controls at day 0 (11 590+/-5080 for PPH patients versus 11 900+/-1790 for control subjects), decreased during treatment (ANOVA, P=0.038) and became significantly low at day 40 (8660+/-3520, P<0.001). The number of CD63 epitopes was not elevated, and P-selectin was never detected at any time point on PPH platelets. This glycoprotein profile indicates that the platelets of PPH patients were not highly activated but had an accelerated turnover and returned to normal under epoprostenol treatment without change of the elevated plasma serotonin, characteristic of PPH. In conclusion, neither platelet activation nor a significant alteration of the 5-HT endothelial metabolism explains the high level of plasma 5-HT in PPH patients. The 5-HT plasma concentration is not a predictive marker of the severity of PPH, and its evolution is independent of the clinical and hemodynamic status. Treatment by a potent antiaggregating agent, ...

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“…22 Expression of CD36 in heart was increased in mice fed a high-fat diet. 27 Michelson et al 28 demonstrated that thrombin activation increases the expression of CD36 on the surface of platelets. Recently, Han et al 29 reported that native and modified LDLs increased the functional expression of CD36 by using J774 murine macrophages.…”

Section: Discussionmentioning

confidence: 99%

Oxidized LDL Increases and Interferon-γ Decreases Expression of CD36 in Human Monocyte–Derived Macrophages

Nakagawa

Nozaki

Nishida

et al. 1998

ATVB

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Abstract-CD36 is a glycoprotein with an M r of 88 kDa that is expressed on platelets, monocytes/macrophages, capillary endothelial cells, and adipocytes. We previously demonstrated that CD36 is involved in the uptake of oxidized low density lipoprotein (OxLDL) by using CD36-deficient macrophages (J Clin Invest. 1995;96:1859). However, the regulation of CD36 expression in human monocyte-derived macrophages has not been fully elucidated. The current study attempted to clarify the effect of OxLDL and cytokines, both of which are present in atherosclerotic lesions and may play an important role in atherogenesis, on the expression of CD36. A cell enzyme-linked immunosorbent assay and flow cytometry were used to detect CD36 protein. A ribonuclease protection assay was used to measure CD36 mRNA in human monocyte-derived macrophages. The expression of CD36 was increased during the differentiation of monocytes to macrophages. Incubation of macrophages with 25 g/mL OxLDL for 24 hours increased the level of CD36 protein by 56% and that of CD36 mRNA by 58%. Lysophosphatidylcholine did not affect the expression of CD36. The effects of OxLDL were demonstrated in macrophages that had already differentiated to the point where CD36 expression was almost maximal. Interferon-␥ (IFN-␥) reduced the expression of CD36 in a dose-dependent manner. A concentration of 1000 U/mL IFN-␥ significantly reduced the expression of CD36 protein by 57% and that of CD36 mRNA by 30%. In conclusion, CD36 may be important in the formation of foam cells by induction through its ligand (OxLDL

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Platelet activation results in a redistribution of glycoprotein IV (CD36).

Cited by 36 publications

References 63 publications

Flow cytometric analysis of platelets from childrenwith the Wiskott‐Aldrich syndrome reveals defects in platelet development, activation and structure

Flow cytometric analysis of platelets from childrenwith the Wiskott‐Aldrich syndrome reveals defects in platelet development, activation and structure

High Plasma Serotonin Levels in Primary Pulmonary Hypertension

Oxidized LDL Increases and Interferon-γ Decreases Expression of CD36 in Human Monocyte–Derived Macrophages

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