M2 Macrophages Participate in the Biological Tissue Healing Reaction to Mineral Trioxide Aggregate
M2 Macrophages Participate in the Biological Tissue Healing Reaction to Mineral Trioxide Aggregate
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DOI：
10.1016/j.joen.2013.11.011
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发表时间：
2014-03-01
影响因子：
4.2
通讯作者：
Okiji, Takashi
中科院分区：
文献类型：
--
作者：
Ito, Takafumi;Kaneko, Tomoatsu;Okiji, Takashi
简介：本研究检测了植入三氧化二矿物质聚集体 (MTA) 的大鼠皮下组织中与 M2（伤口愈合）巨噬细胞相关分子的蛋白质和信使 RNA (mRNA) 表达，以阐明 M2 巨噬细胞参与结缔组织对 MTA 的反应。方法：将含有新鲜混合的 MTA 或氢氧化钙水泥（Life；Kerr，Romulus，MI）的硅胶管皮下植入 Wistar 大鼠的背部。植入不同动物体内的固体硅胶棒作为对照。然后对样本进行 ED1（CD68，一种通用巨噬细胞标记物）和 ED2（CD163，一种 M2 巨噬细胞标记物）的双重免疫染色。还进行了 CD34（血管化和伤口愈合的标记物）的免疫染色。 CD34、CD163 和甘露糖受体 c 型 1（M2 巨噬细胞标记物）mRNA 的表达水平通过实时聚合酶链式反应测定。结果：与 Life 植入组织和对照组织相比，MTA 植入皮下组织显示植入部位下方 ED1+ED2+ 巨噬细胞密度以及 CD163 和 MMR mRNA 表达水平显着增加。与 Life 植入组织和对照组织相比，MTA 植入皮下组织还显示 CD34 免疫染色区域显着增加，CD34 mRNA 上调。结论：MTA植入诱导了表达M2巨噬细胞标志物（ED2）的巨噬细胞的积累，并增强了M2巨噬细胞标志物基因的表达。 MTA 植入还增强了 CD34 的表达，表明愈合/组织修复过程加速。总而言之，生物结缔组织对 MTA 的反应可能涉及涉及 M2 巨噬细胞的伤口愈合/组织修复过程。
Introduction: This study examined the protein and messenger RNA (mRNA) expression of molecules associated with M2 (wound healing) macrophages in mineral trioxide aggregate (MTA)-implanted rat subcutaneous tissue to elucidate the involvement of M2 macrophages in the connective tissue response to MTA. Methods: Silicone tubes containing freshly mixed MTA or a calcium hydroxide cement (Life; Kerr, Romulus, MI) were subcutaneously implanted into the backs of Wistar rats. Solid silicone rods implanted in different animals served as controls. The specimens were then double immunostained for ED1 (CD68, a general macrophage marker) and ED2 (CD163, an M2 macrophage marker). Immunostaining for CD34 (a marker for vascularization and wound healing) was also performed. Expression levels of CD34, CD163, and mannose receptor c type 1 (an M2 macrophage marker) mRNAs were determined with real-time polymerase chain reaction. Results: MTA-implanted subcutaneous tissues showed significant increases in the density of ED1+ED2+ macrophages beneath the implantation site and expression levels of CD163 and MMR mRNAs compared with Life-implanted and control tissues. MTA-implanted subcutaneous tissues also showed a significant increase of CD34-immunostained areas and up-regulation of CD34 mRNAs compared with Life-implanted and control tissues. Conclusions: MTA implantation induced the accumulation of M2 macrophage marker (ED2)-expressing macrophages and enhanced the expression of M2 macrophage marker genes. MTA implantation also enhanced the expression of CD34, suggesting acceleration of the healing/tissue repair process. Taken together, biological connective tissue response to MTA may involve wound healing/tissue repair processes involving M2 macrophages.