Mehrpouri Mahdieh, Bashash Davood, Mohammadi Mohammad Hossien, Gheydari Mohammad Esmail, Satlsar Esmail Shahabi, Hamidpour Mohsen
Shahid Beheshti University of Medical Sciences, Faculty of Allied Medical Sciences, Department of Hematology and Blood Banking, Tehran, Iran
HSCT Research Centre, Department of Hematology and Blood Banking, School of Allied Medical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Turk J Haematol. 2019 May 3;36(2):97-105. doi: 10.4274/tjh.galenos.2019.2018.0449. Epub 2019 Mar 12.
Far beyond hemostasis and thrombosis, significant evidence has indicated the critical role of platelets in atherosclerosis. SDF-1 is among the pro-inflammatory chemokines that are increased in platelets of patients with coronary artery disease (CAD). The goal of the current work is to identify the in vitro effect of platelets from either CAD patients or healthy volunteers on the induction of macrophages and foam cells.
The expression of SDF-1 on platelet surfaces in CAD patients and healthy volunteers was investigated using flow cytometry. We also evaluated the CXCR4/CXCR7 expression on monocytes from buffy coats of healthy volunteers. The effect of platelets from CAD patients and healthy volunteers on differentiation of monocytes and foam cell formation was evaluated using Oil Red O (ORO) staining. Flow cytometry and real-time PCR were also employed to evaluate surface markers and mRNA expression of genes involved in this process after co-culture of platelets with monocytes.
Monocytes in co-culture with platelets acquired a spindleshape appearance and ORO-positive lipid droplets. In addition, platelets could induce CD163 expression, as an important marker of M2 macrophage, and upregulate the mRNA expression of the , and genes in monocytes. Notably, platelets of CAD patients with higher expression of SDF-1, increased the expression of genes encoding SRB and CD36 as compared to platelets of healthy volunteers.
Our results indicate that platelets from CAD patients could provoke monocyte differentiation into macrophages with an M2 phenotype, which in turn may participate in an atheroprotective process.
大量证据表明，血小板在动脉粥样硬化中的作用远不止止血和血栓形成。基质细胞衍生因子-1（SDF-1）是冠心病（CAD）患者血小板中升高的促炎趋化因子之一。本研究旨在确定CAD患者或健康志愿者的血小板在体外对巨噬细胞和泡沫细胞诱导的影响。
采用流式细胞术研究CAD患者和健康志愿者血小板表面SDF-1的表达。我们还评估了健康志愿者血沉棕黄层中单核细胞上CXCR4/CXCR7的表达。采用油红O（ORO）染色评估CAD患者和健康志愿者血小板对单核细胞分化和泡沫细胞形成的影响。在血小板与单核细胞共培养后，还采用流式细胞术和实时定量PCR评估参与此过程的基因的表面标志物和mRNA表达。
与血小板共培养的单核细胞呈现纺锤形外观和ORO阳性脂滴。此外，血小板可诱导作为M2巨噬细胞重要标志物的CD163表达，并上调单核细胞中、和基因的mRNA表达。值得注意的是，与健康志愿者的血小板相比，SDF-1表达较高的CAD患者血小板增加了编码清道夫受体B（SRB）和CD36的基因的表达。
我们的结果表明，CAD患者的血小板可促使单核细胞分化为具有M2表型的巨噬细胞，这反过来可能参与动脉粥样硬化的保护过程。
