Cytokine mRNA expression in human platelets and a megakaryocytic cell line and cytokine modulation of platelet function
Cytokine mRNA expression in human platelets and a megakaryocytic cell line and cytokine modulation of platelet function
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DOI：
10.1006/cyto.1996.0182
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发表时间：
1997-06-01
期刊：
影响因子：
3.8
通讯作者：
Wang, Y
中科院分区：
文献类型：
--
作者：
Soslau, G;Morgan, DA;Wang, Y
在体内，血小板的形成和功能受到微环境中细胞因子的不同程度的调节。虽然白细胞是心血管系统中细胞因子的主要来源，但这项研究涉及的问题是，血小板和血小板前体--巨核细胞--是否也可能是细胞因子的来源。血小板产生或携带的细胞因子可在血管损伤部位释放，参与伤口愈合。血小板和人巨核细胞系HU3表达白介素7(IL-7)、干细胞因子(SCF)、转化生长因子β(TGF-β)、cMp1、IgE受体亚基Fc epsilon RLα-Gamma和转录因子NF-E2。其他在HU3细胞中表达但在血小板中不表达的细胞因子包括IL-1β、IL-6、IL-IO、IL-13、TNF-α和Fc epsilon RIβ亚基。HU3细胞系似乎比第二个血液来源的双潜能细胞系MBO2在血小板形成的成熟/分化途径上走得更远。MBO2细胞株不表达IL-6、IL-10、SCF、TNF-α和cMp1。此外，在TPO中培养HU3细胞似乎抑制了Fc epsilon RIβ的表达，使细胞更接近于血小板表型。根据细胞因子在血小板/巨核细胞中的表达，在添加细胞因子的情况下，测定激动剂诱导的血小板聚集，以此作为评估细胞因子对血小板功能的潜在调节的手段。IL-6、SCF和TPO可显著促进胶原诱导的聚集。其他细胞因子显著刺激凝血酶受体激活肽、SFLLRNP-、U46619-和ADP诱导的血小板聚集，其中TPO是最一致的激活剂。从血小板释放的细胞因子可能与从其他细胞来源释放的细胞因子协同作用，根据损伤部位的不同而调节止血和血栓形成。(C)1997年学术出版社有限公司。
Platelet formation and function are regulated, in vivo, to varying degrees by cytokines in the micro-environment. While white blood cells are the major source of cytokines within the cardiovascular system, the question addressed in this study was whether platelets and the platelet precursor, the megakaryocyte, may also serve as a source of cytokines. Cytokines produced by or carried within platelets could be released at sites of vascular injury and participate in wound healing. Platelets and a human megakaryocyte-like cell line, HU3, were found to express message for interleukin 7 (IL-7), stem cell factor (SCF), transforming growth factor beta (TGF-beta), cMpl, the IgE receptor subunits Fc epsilon Rl alpha gamma and the transcription factor, NF-E2. Other cytokines expressed in HU3 cells but not in platelets included IL-1 beta, IL-6, IL-IO, IL-13, TNF-alpha and the Fc epsilon RI beta subunit. The HU3 cell line seemed to be further along the maturation/differentiation pathway to platelet formation than a second blood derived bipotential cell line, MBO2. The MBO2 cell line did not express IL-6, IL-10, SCF, TNF-alpha nor cMpl. Furthermore, culturing the HU3 cells in TPO appeared to repress expression of Fc epsilon RI beta directing the cell closer to the platelet phenotype. In light of the presence of cytokine expression in platelets/megakaryocytes, agonist-induced platelet aggregation was measured in the presence of added cytokines as a means to evaluate potential cytokine modulation of platelet function. Collagen-induced aggregations were significantly enhanced by IL-6, SCF and TPO. Other cytokines tested significantly stimulated the thrombin receptor activating peptide, SFLLRNP-, U46619- and ADP-induced platelet aggregations with TPO being the most consistent activator. It is possible that cytokines released from platelets act in concert with cytokines released from other cellular sources to modulate haemostasis and thrombosis differentially depending upon the site of injury. (C) 1997 Academic Press Limited.