Menschikowski M, Kasper M, Lattke P, Schiering A, Schiefer S, Stockinger H, Jaross W
Institute of Clinical Chemistry, Faculty of Medicine Carl Gustav Carus, Technical University of Dresden, Germany.
Atherosclerosis. 1995 Dec;118(2):173-81. doi: 10.1016/0021-9150(95)05604-1.
Atherosclerotic plaques exhibit a series of features that are similar to those of chronic inflammation. Based on the fact that during inflammation several cell types synthesize and secrete a group II phospholipase A2 (PLA2), an immunohistochemical study was undertaken to explore whether this enzyme can be identified in human atherosclerotic lesions. Tissue specimens obtained from 13 patients who had undergone arteriectomy and three specimens with advanced atherosclerotic plaques obtained at autopsy were analyzed and compared to arteries free of atherosclerosis. The results showed that in all areas with atherosclerotic lesions, a staining with monoclonal antibodies raised against group II PLA2 was evident. In normal arteries without thickened intima, this immunostaining was completely negative. With the use of specific monoclonal antibodies against macrophages (anti-KP-1) and smooth muscle cells (anti-alpha-actin), PLA2-positive cells were identified as foam cells mainly derived from macrophages. In addition to these cells, other regions of the thickened intima gave a partially positive reaction with anti-PLA2 antibodies, but could not be stained with either anti-KP-1 or anti-alpha-actin. Some of these regions were localized on edges of calcification and cell necrosis. Other PLA2-positive regions seem to be associated with extracellular matrix structures. In summary, the findings of this study may be regarded as further evidence to support the link between atherosclerosis and chronic inflammatory processes. In view of the fact that the in vitro modification of lipoproteins by PLA2-treatment induces lipid deposition in macrophages, the results of this study suggest that group II PLA2 may actively be involved in the formation of foam cells in vivo.
动脉粥样硬化斑块呈现出一系列与慢性炎症相似的特征。基于炎症过程中几种细胞类型可合成并分泌II型磷脂酶A2（PLA2）这一事实，开展了一项免疫组织化学研究，以探究该酶是否可在人类动脉粥样硬化病变中被识别。对13例接受动脉切除术患者的组织标本以及3例尸检时获取的晚期动脉粥样硬化斑块标本进行了分析，并与无动脉粥样硬化的动脉进行比较。结果显示，在所有有动脉粥样硬化病变的区域，用针对II型PLA2产生的单克隆抗体进行染色均呈阳性。在无内膜增厚的正常动脉中，这种免疫染色完全为阴性。利用针对巨噬细胞（抗KP-1）和平滑肌细胞（抗α-肌动蛋白）的特异性单克隆抗体，PLA2阳性细胞被鉴定为主要源自巨噬细胞的泡沫细胞。除这些细胞外，内膜增厚的其他区域对抗PLA2抗体呈部分阳性反应，但不能被抗KP-1或抗α-肌动蛋白染色。其中一些区域位于钙化和细胞坏死边缘。其他PLA2阳性区域似乎与细胞外基质结构有关。总之，本研究结果可被视为支持动脉粥样硬化与慢性炎症过程之间联系的进一步证据。鉴于PLA2处理对脂蛋白进行体外修饰可诱导巨噬细胞内脂质沉积，本研究结果表明II型PLA2可能在体内泡沫细胞的形成过程中发挥积极作用。
