| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on December 18, 2008
Accepted on April 7, 2009
RIIa by Interferon
From the Cardiology Unit, and Cardiovascular Research Institute, Department of Medicine, University of Vermont, Burlington.
* To whom correspondence should be addressed. E-mail: david.schneider{at}uvm.edu.
Objective—The purpose of this study was to identify factors that alter expression of Fc
RIIa by megakaryocytes.
Methods and Results—Effects of selected cytokines and growth factors on megakaryocyte expression of Fc
RIIa 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 Fc
RIIa 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)
increased protein expression of Fc
RIIa by HEL cells and CD34 stem cells after megakaryocyte differentiation (maximal
4-fold, P<0.001 for each). IFN
did not increase expression of Fc
RIIa by undifferentiated HEL and CD34 cells. Expression of Fc
RIIa mRNA was increased (2-fold, P<0.001) in megakaryocyte-differentiated HEL cells. IFN
did not increase expression of Fc
RIIa by undifferentiated myelocytic or monocytic cell lines.
Conclusions—IFN
appears to selectively increase expression of Fc
RIIa by cells exhibiting characteristics of megakaryocytes. This effect of IFN
may contribute to greater platelet expression of Fc
RIIa in patients with atherosclerotic vascular disease.
R
inflammation
platelets
megakaryocytes
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2009 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |