人们对血小板的认识都一向简单：这是一种没有细胞核的血细胞，比其他的血细胞要小，因为能够帮助在伤口快速形成凝块并防止干扰而小有名气。最近，一向“表现良好”的血小板似乎和慢性炎症扯上了关系，不过关系并不清楚。
在快速在线发表的《血液》杂志上，University of Rochester的研究者展示了血小板的不为人知另一面。他们相信，这个小东西在炎症、心脏病和中风间起到了枢纽的作用；甚至还是体内促发糖尿病并发症的关键细胞。
研究发现，血小板含有高水平的过氧化物酶增殖体活化受体γ （Peroxisome Proliferator Activated Receptor gamma，PPARgamma），一种对脂类代谢、糖尿病以及炎症重要的转录因子。血小板的过氧化物酶增殖体活化受体γ 是有活性的，因为过氧化物酶增殖体活化受体γ的激活剂（agonist）可以减弱血小板的活化，特别是阻碍CD40配体（CD40 Ligand, CD40L）的释放。而已经知道，血液中的CD40L水平和炎症、动脉粥样化症、糖尿病都有关。
无核的细胞通常被认为功能较简单，看来血小板远比我们所想象的来得复杂。
http://www.urmc.rochester.edu/pr/news/story.cfm?id=551
| Blood. 2004 May 6 |
Human bone marrow megakaryocytes and platelets express PPAR{gamma} and PPAR{gamma} agonists blunt platelet release of CD40 ligand and thromboxanes.
Akbiyik F, Ray DM, Gettings KF, Blumberg N, Francis CW, Phipps RP.
Biochemistry, Hacettepe University, Ankara, Turkey; Environmental Medicine, Microbiology and Immunology, and the Lung Biology and Disease Program, University of Rochester, Rochester, NY, USA.
Peroxisome Proliferator Activated Receptor gamma (PPARgamma) is a ligand-activated transcription factor important in lipid metabolism, diabetes, and inflammation. We evaluated whether human platelets and megakaryocytes express PPARgamma and whether PPARgamma agonists influence platelet release of bioactive mediators. Although PPARgamma is mainly considered a nuclear receptor, we show that enucleate platelets highly express PPARgamma protein as shown by western blotting, flow cytometry, and immunocytochemistry. Meg-01 megakaryocyte cells and human bone marrow megakaryocytes also express PPARgamma. Platelet and Meg-01 PPARgamma bound the PPARgamma DNA consensus sequence and this was enhanced by PPARgamma agonists. Platelets are not only essential for clotting, but have an emerging role in inflammation in part due to their release or production of the pro-inflammatory and pro-atherogenic mediators CD40 ligand (L) and thromboxanes (TX). Platelet incubation with a natural PPARgamma agonist, 15d-PGJ2, or with a potent synthetic PPARgamma ligand, rosiglitazone, prevented thrombin-induced CD40L surface expression and release of CD40L and TXB2. 15d-PGJ2 also inhibited platelet aggregation and ATP release. Our results show that human platelets express PPARgamma and that PPARgamma agonists such as the thiazolidinedione class of anti-diabetic drugs have a new target cell, the platelet. This may represent a novel mechanism for treatment of inflammation, thrombosis and vascular disease in high-risk patients.
