Daub Karin, Langer Harald, Seizer Peter, Stellos Konstantinos, May Andreas E, Goyal Pankaj, Bigalke Boris, Schönberger Tanja, Geisler Tobias, Siegel-Axel Dorothea, Oostendorp Robert A J, Lindemann Stephan, Gawaz Meinrad
Medizinische Klinik III, Eberhard Karls Universität Tübingen, Tübingen, Germany.
FASEB J. 2006 Dec;20(14):2559-61. doi: 10.1096/fj.06-6265fje. Epub 2006 Oct 31.
Recruitment of human CD34+ progenitor cells toward vascular lesions and differentiation into vascular cells has been regarded as a critical initial step in atherosclerosis. Previously we found that adherent platelets represent potential mediators of progenitor cell homing besides their role in thrombus formation. On the other hand, foam cell formation represents a key process in atherosclerotic plaque formation. To investigate whether platelets are involved in progenitor cell recruitment and differentiation into endothelial cells and foam cells, we examined the interactions of platelets and CD34+ progenitor cells. Cocultivation experiments showed that human platelets recruit CD34+ progenitor cells via the specific adhesion receptors P-selectin/PSGL-1 and beta1- and beta2-integrins. Furthermore, platelets were found to induce differentiation of CD34+ progenitor cells into mature foam cells and endothelial cells. Platelet-induced foam cell generation could be prevented partially by HMG coenzyme A reductase inhibitors via reduction of matrix metalloproteinase-9 (MMP-9) secretion. Finally, agonists of peroxisome proliferator-activated receptor-alpha and -gamma attenuated platelet-induced foam cell generation and production of MMP-9. The present study describes a potentially important mechanism of platelet-induced foam cell formation and generation of endothelium in atherogenesis and atheroprogression. The understanding and modulation of these mechanisms may offer new treatment strategies for patients at high risk for atherosclerotic diseases.
人类CD34+祖细胞向血管病变部位募集并分化为血管细胞,被认为是动脉粥样硬化关键的起始步骤。此前我们发现,黏附血小板除了在血栓形成中发挥作用外,还是祖细胞归巢的潜在介质。另一方面,泡沫细胞形成是动脉粥样硬化斑块形成的关键过程。为了研究血小板是否参与祖细胞向内皮细胞和泡沫细胞的募集及分化,我们检测了血小板与CD34+祖细胞之间的相互作用。共培养实验表明,人血小板通过特异性黏附受体P-选择素/PSGL-1以及β1和β2整合素募集CD34+祖细胞。此外,还发现血小板可诱导CD34+祖细胞分化为成熟的泡沫细胞和内皮细胞。HMG辅酶A还原酶抑制剂可通过减少基质金属蛋白酶-9(MMP-9)分泌,部分阻止血小板诱导的泡沫细胞生成。最后,过氧化物酶体增殖物激活受体-α和-γ激动剂可减弱血小板诱导的泡沫细胞生成及MMP-9的产生。本研究描述了血小板诱导的泡沫细胞形成及动脉粥样硬化发生发展过程中内皮生成的一个潜在重要机制。对这些机制的理解和调控可能为动脉粥样硬化疾病高危患者提供新的治疗策略。