Affiliation:
1. From the Cardiology Unit, and Cardiovascular Research Institute, Department of Medicine, University of Vermont, Burlington.
Abstract
Objective—
The purpose of this study was to identify factors that alter expression of FcγRIIa by megakaryocytes.
Methods and Results—
Effects of selected cytokines and growth factors on megakaryocyte expression of FcγRIIa were assessed with phorbol 12-myristate 13-acetate (PMA)-differentiated human erythroleukemia (HEL) cells and with thrombopoietin-differentiated CD34 stem cells and compared with those obtained with myelocytic cell lines and a monocytic cell lines. Expression of FcγRIIa was quantified with the use of Western blots and real-time reverse transcriptase-polymerase chain reaction. Megakaryocyte differentiation was identified by expression of CD41, CD42, and von Willebrand factor with the use of flow cytometry. Interferon (IFN) γ increased protein expression of FcγRIIa by HEL cells and CD34 stem cells after megakaryocyte differentiation (maximal ≈4-fold,
P
<0.001 for each). IFNγ did not increase expression of FcγRIIa by undifferentiated HEL and CD34 cells. Expression of FcγRIIa mRNA was increased (2-fold,
P
<0.001) in megakaryocyte-differentiated HEL cells. IFNγ did not increase expression of FcγRIIa by undifferentiated myelocytic or monocytic cell lines.
Conclusions—
IFNγ appears to selectively increase expression of FcγRIIa by cells exhibiting characteristics of megakaryocytes. This effect of IFNγ may contribute to greater platelet expression of FcγRIIa in patients with atherosclerotic vascular disease.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Cardiology and Cardiovascular Medicine
Cited by
10 articles.
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