Oral malodorous compound inhibits osteoblast proliferation.
Oral malodorous compound inhibits osteoblast proliferation.
复制标题
口腔恶臭化合物抑制成骨细胞增殖。
DOI：
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Takeshi Kamoda
中科院分区：
文献类型：
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作者：
T. Imai;Hisataka Ii;K. Yaegaki;T. Murata;Tsutomu Sato;Takeshi Kamoda
背景
包括硫化氢 (H2S) 在内的口腔恶臭化合物是牙周炎的病原体，因为其毒性与氰酸盐类似。先前的研究表明，挥发性硫化合物（VSC）对牙周组织具有剧毒，导致人牙龈成纤维细胞和细胞外基质中胶原蛋白的量大幅减少，以及细胞凋亡、免疫反应和基质金属蛋白酶的产生等。本研究的目的是确定 H2S 对成骨细胞增殖的影响以及通过丝裂原激活蛋白激酶 (MAPK) 的信号转导途径。
方法
将正常人成骨细胞 (NHOst) 和鼠成骨细胞（细胞系 MC3T3-E1）与 H2S 一起孵育。通过测量[3H]胸苷掺入来评估细胞增殖。通过蛋白质印迹分析确定细胞外信号调节激酶 (ERK)1/2 和 p38 磷酸化，在 NHOst 中评估 H2S 对控制细胞增殖的信号转导途径（MAPK 级联）的影响。
结果
将 NHOst 与 H2S 孵育 24 小时后，[3H]胸苷掺入 DNA 的量显着减少，且与 H(2)S 呈剂量依赖性。在 H2S 浓度为 100 ng/ml 时，[3H]胸苷掺入量与对照相比减少了 79%。从 MC3T3-E1 获得了类似的结果。开始治疗后 10 分钟，ERK1/2 和 p38 的磷酸化因 H2S 增加，然后随时间依赖性下降。 H2S 诱导的 ERK1/2 和 p38 的激活被 MAPK/ERK 激酶 ([MEK]; U0126) 或 p38 (SB203580) 的特异性抑制剂抑制。
结论
H2S通过MAPK途径抑制人成骨细胞的增殖。
BACKGROUND
Oral malodorous compounds including hydrogen sulfide (H2S) are causative agents of periodontitis because the toxicities are similar to that of cyanate. Previous studies demonstrated that volatile sulfur compounds (VSCs) were highly toxic to periodontal tissues, causing a large reduction in the amount of collagen in human gingival fibroblasts and extracellular matrix as well as, for example, apoptosis, immunologic responses, and matrix metalloproteinase production. The objective of this study was to determine the effect of H2S on the proliferation of osteoblasts and a signaling transduction pathway through the mitogen-activated protein kinase (MAPK).
METHODS
Normal human osteoblasts (NHOst) and murine osteoblasts (cell line MC3T3-E1) were incubated with H2S. Cell proliferation was assessed by measuring [3H]thymidine incorporation. The effects of H2S on the signal transduction pathways, the MAPK cascade, that control cell proliferation were evaluated in NHOst by determining extracellular signal-regulated kinase (ERK)1/2 and p38 phosphorylation with a Western blot analysis.
RESULTS
After incubating NHOst with H2S for 24 hours, [3H]thymidine incorporation into the DNA significantly decreased dose-dependently with H(2)S. At a concentration of 100 ng/ml H2S, [3H]thymidine incorporation decreased 79% compared to the control. Similar results were obtained from MC3T3-E1. The phosphorylation of ERK1/2 and p38 was increased by H2S at 10 minutes after starting the treatment and then decreased time dependently. The activation of ERK1/2 and p38 induced by H2S was inhibited by the specific inhibitor of MAPK/ERK kinase ([MEK]; U0126) or p38 (SB203580).
CONCLUSION
H2S inhibited the proliferation of human osteoblastic cells through the MAPK pathway.
影响因子：
3.5
作者：
Johnson,P;Yaegaki,K;Tonzetich,J
通讯作者：
Tonzetich,J