Division of Oral Rehabilitation, Department of Endodontology and Operative Dentistry, Faculty of Dental Science, Kyushu University, Fukuoka 812-8582, Japan.
J Dent Res. 2011 Feb;90(2):181-5. doi: 10.1177/0022034510382118.
The loading caused by occlusion and mastication plays an important role in maintaining periodontal ligament (PDL) tissues. We hypothesized that a loading magnitude would be involved in the production of biological factors that function in the maintenance of PDL tissues. Here, we identified up-regulated gene expressions of transforming growth factor-β1 (TGF-β1), alkaline phosphatase (ALP), and angiotensinogen in human PDL fibroblastic cells (HPLFs) that were exposed to 8% stretch loading. Immunolocalization of angiotensin I/II (Ang I/II), which was converted from angiotensinogen, was detected in rat PDL tissues. HPLFs that were stimulated by Ang II also increased their gene expressions of TGF-β1 and ALP. Furthermore, the antagonist for Ang II type 2 receptor, rather than for type 1, significantly inhibited gene expressions induced by the stretch loading. Analysis of these data suggests that Ang II mediates the loading signal in stretched HPLFs to induce expressions of TGF-β1 and ALP.
闭塞和咀嚼引起的负荷对维持牙周韧带（PDL）组织起着重要作用。我们假设，在产生生物因子的过程中，会涉及到一个负荷量，这些生物因子在维持 PDL 组织的功能中发挥作用。在这里，我们发现，在暴露于 8%拉伸负荷的人牙周成纤维细胞（HPLF）中，转化生长因子-β1（TGF-β1）、碱性磷酸酶（ALP）和血管紧张素原的基因表达上调。血管紧张素原转化而来的血管紧张素 I/II（Ang I/II）在大鼠 PDL 组织中的免疫定位被检测到。受 Ang II 刺激的 HPLF 也增加了它们的 TGF-β1 和 ALP 基因表达。此外，血管紧张素 II 型 2 受体拮抗剂，而不是 1 型拮抗剂，显著抑制了拉伸负荷诱导的基因表达。对这些数据的分析表明，Ang II 介导拉伸 HPLF 中的负荷信号，诱导 TGF-β1 和 ALP 的表达。
