Liu Dawen, Wise Gary E
Department of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA 70803, USA.
Eur J Oral Sci. 2008 Aug;116(4):334-40. doi: 10.1111/j.1600-0722.2008.00547.x.
Endothelial monocyte-activating polypeptide II (EMAP-II) is an inflammatory cytokine with chemotactic activity. Because the dental follicle (DF) recruits mononuclear cells (osteoclast precursors) to promote the osteoclastogenesis needed for tooth eruption, it was the aim of this study to determine if EMAP-II contributes to this recruitment. Using a DNA microarray, EMAP-II was found to be highly expressed in vivo in the DFs of day 1 to day 11 postnatal rats, with its expression elevated on days 1 and 3. Use of a short interfering RNA (siRNA) to knock down EMAP-II expression resulted in a reduction in the expression of colony-stimulating factor-1 (CSF-1) and monocyte chemoattractant protein-1 (MCP-1) in the DF cells. Addition of EMAP-II protein to the DF cells partially restored the expression of CSF-1 and MCP-1. In chemotaxis assays using either conditioned medium of the DF cells with anti-(EMAP-II) immunoglobulin G added or conditioned medium of DF cells with EMAP-II knocked down by siRNA, migration indexes of bone marrow mononuclear cells were significantly reduced. These results suggest that EMAP-II is another chemotactic molecule in the dental follicle involved in the recruitment of mononuclear cells, and that EMAP-II may exert its chemotactic function directly by recruiting mononuclear cells and indirectly by enhancing the expression of other chemotactic molecules (CSF-1 and MCP-1).
内皮单核细胞激活多肽II（EMAP-II）是一种具有趋化活性的炎性细胞因子。由于牙囊（DF）招募单核细胞（破骨细胞前体）以促进牙齿萌出所需的破骨细胞生成，因此本研究的目的是确定EMAP-II是否参与了这一招募过程。通过DNA微阵列分析发现，EMAP-II在出生后1至11天大鼠的牙囊中高表达，在第1天和第3天表达升高。使用小干扰RNA（siRNA）敲低EMAP-II的表达导致牙囊细胞中集落刺激因子-1（CSF-1）和单核细胞趋化蛋白-1（MCP-1）的表达降低。向牙囊细胞中添加EMAP-II蛋白可部分恢复CSF-1和MCP-1的表达。在趋化性分析中，使用添加了抗（EMAP-II）免疫球蛋白G的牙囊细胞条件培养基或使用经siRNA敲低EMAP-II的牙囊细胞条件培养基，骨髓单核细胞的迁移指数均显著降低。这些结果表明，EMAP-II是牙囊中另一种参与单核细胞招募的趋化分子，并且EMAP-II可能通过直接招募单核细胞以及间接增强其他趋化分子（CSF-1和MCP-1）的表达来发挥其趋化功能。
