• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Open Journal of Urology >Influence of Adiponectin and Leptin on the Kinetics of Human Pulp Cells
【24h】

Influence of Adiponectin and Leptin on the Kinetics of Human Pulp Cells

机译：脂联素和瘦素对人牙髓细胞动力学的影响

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Adipocytokines, such as adiponectin and leptin, are expressed by adipocytes and are known as anti-metabolic syndrome factors. They are also thought to mediate calcification in mineralized tissue. We investigated the effects of adiponectin and leptin on the kinetics of human pulp cells using ELISA and western blot. After gaining informed consent, we obtained human pulp cells from three patients. After cultivation in Dulbecco’s Modified Eagle Medium (DMEM) without serum, cells from the 4th to 6th passages were incubated with various concentrations of adiponectin (1, 10, or 100 ng/mL) in DMEM or leptin (0.1, 1, or 10 ng/mL) in DMEM for 24 h. We confirmed that human pulp cells expressed adiponectin receptor 1 and leptin receptor. Although the proliferation index of these cells as measured by 5-bromo-2'-deoxyuridine (BrdU) incorporation increased in the presence of adiponectin in a dose-de pendent manner, pulp cells stimulated with leptin showed no significant changes in BrdU incorporation. Alkaline phosphatase activity showed no significant changes after stimulation with either adipocytokine. Adiponectin induced expression of BMP-2 and osteopontin more strongly than did leptin. In particular, expression of BMP-2 increased in the presence of adiponectin i n a dose-dependent manner. In contrast, the expression of dentin sialopr otein increased after stimulation with leptin. The expression of Runx2 was not observed from the cultured pulp cells stimulated with both molecules. These results indicate that adiponectin and leptin contribute to growth and differentiation of human pulp cells and may consequently affect the formation of secondary dentin or reparative dentin in the dentin-pulp complex.
机译：adipocytokines，例如脂联素和瘦素，被脂肪细胞表达，称为抗代谢综合征因子。他们也被认为在矿化组织中调解钙化。我们研究了ELISA和Western印迹的脂联素和瘦素对人牙髓细胞动力学的影响。在获得知情同意之后，我们从三名患者获得人纸浆细胞。在没有血清的Dulbecco的改性鹰培养基（DMEM）中，将来自第4至第6次通道的细胞在DMEM或瘦蛋白中与各种浓度的脂联素（1,10或100ng / ml）一起温育（0.1,1或10 ng / ml）在DMEM中24小时。我们证实人纸浆细胞表达了脂联素受体1和瘦素受体。虽然通过5-溴-2'-脱氧尿苷（BRDU）掺入的这些细胞的增殖指数在脂联素的存在下以剂量 - de悬垂方式增加，用瘦蛋白刺激的纸浆细胞显示BRDU掺入没有显着变化。碱性磷酸酶活性在用脂肪细胞因子刺激后没有显着变化。脂联素诱导BMP-2和骨桥蛋白的表达比瘦素更强烈。特别地，BMP-2的表达在脂联素I n的存在下增加了剂量依赖性的方式。相比之下，用瘦蛋白刺激后牙本质Sialprotin的表达增加。未从用两种分子刺激的培养的纸浆细胞中观察到runx2的表达。这些结果表明脂联素和瘦素有助于人纸浆细胞的生长和分化，因此可能影响牙本质 - 纸浆复合物中的继发牙本质或牙本质的形成。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号