Mechanical tension alters semaphorin expression in the periodontium.
Mechanical tension alters semaphorin expression in the periodontium.
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DOI：
10.1902/jop.2009.090212
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发表时间：
2009-10
影响因子：
4.3
通讯作者：
Amber Spencer;T. Lallier
中科院分区：
文献类型：
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作者：
Amber Spencer;T. Lallier
背景牙周病重塑需要协调的细胞运动。脑信号蛋白是调节细胞迁移的细胞表面信号，并且可能受到牙周细胞的差异调节。机械张力可以调节牙周膜的改建。我们预测，机械张力改变的semaphorins在牙周组织中的子集的表达可能是最参与调节该组织的重塑。方法将牙周膜细胞和牙龈细胞暴露于机械张力下，观察其在胶原基质上的附着和运动。半定量逆转录-聚合酶链反应监测细胞外基质和脑信号蛋白转录表达的变化。结果机械张力诱导牙周膜成纤维细胞破骨细胞调节基因表达的程度大于牙龈成纤维细胞，骨保护素表达增加，核因子-κ B配体受体激活因子表达减少。这些机械力减少PDL细胞混合，而不改变细胞附着或运动性。同时，这些力量诱导PDL细胞中的几种脑信号蛋白分子发生动态变化，增加脑信号蛋白3D和5 B，减少脑信号蛋白7A。此外，丛蛋白转录表达改变，减少丛蛋白A1和增加丛蛋白C1。这些变化与牙龈成纤维细胞中观察到的变化不同。结论：这些数据表明，一个子集的semaphorins和plexins的动态调节的PDL。由于这些分子可能参与细胞导向，因此信号蛋白的变化可能在牙周重塑中发挥关键作用，影响血管生成或PDL细胞侵入损伤部位。
BACKGROUND Periodontal remodeling requires coordinated cell movement. Semaphorins are cell-surface signals that regulate cell migration and may be differentially regulated by periodontal cells. Mechanical tension can regulate periodontal ligament (PDL) remodeling. We predicted that mechanical tension alters the expression of the subset of semaphorins in the periodontium likely to be most involved with regulating the remodeling of this tissue. METHODS PDL and gingival cells were exposed to mechanical tension, and their attachment and movement on collagen matrices were evaluated. Alterations in extracellular matrix and semaphorin transcript expression were monitored by semiquantitative reverse transcription-polymerase chain reaction. RESULTS Mechanical tension induced osteoclast regulatory transcripts in the PDL cells to a greater extent than gingival fibroblasts, increasing the expression of osteoprotegerin and decreasing receptor activator of nuclear factor-kappa B ligand. These mechanical forces reduced PDL cell mingling, without altering cell attachment or motility. Concurrently, these forces induced dynamic changes in several semaphorin molecules in PDL cells, increasing semaphorin 3D and 5B and decreasing semaphorin 7A. In addition, plexin transcript expression was altered, decreasing plexin A1 and increasing plexin C1. These changes were different than those observed in gingival fibroblasts. CONCLUSIONS These data suggest that a subset of semaphorins and plexins are dynamically regulated in the PDL. Because these molecules may be involved in cell guidance, changes in semaphorins may play a pivotal role in periodontal remodeling, affecting angiogenesis or PDL cell invasion into sites of injury.