Wang Feng-Ming, Hu Tao, Zhou Xuedong
Key Laboratory of Oral Biomedical Engineering, Ministry of Education, Sichuan University, Chengdu, China.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006 Jul;102(1):114-8. doi: 10.1016/j.tripleo.2005.08.007. Epub 2006 Feb 17.
The objective of this study was to investigate the implication of p38 mitogen-activated protein kinase (MAPK) in mediating alkaline phosphatase (ALPase) activity in human dental pulp cells (HPCs).
Nuclear translocation of p38 was observed by immunofluorescence in isolated HPCs treated with transforming growth factor beta1 (TGF-beta1). TGF-beta1 was used to examine the interaction between p38 MAPK and Smad pathway. Role of p38 kinase in mediating ALPase activity was determined with SB203580, a specific inhibitor for the p38 pathway. Lipopolysaccharide (LPS) or TGF-beta1 was added to inhibit or increase ALPase activity. Statistical analysis was performed by unpaired t test.
TGF-beta1 induced nuclear translocalization of p38. Blockage of p38 pathway with SB203580 inhibited translocation of Smad2/3 to nuclei. ALPase activity decreased in cells treated with SB203580, in contrast to its vehicle (P < .05). Inhibition on enzyme activity by LPS was exacerbated by SB203580 (P < .05). Treatment with SB203580 before addition of TGF-beta1 also made a significant decrease in ALPase activity (P < .05).
These results suggest that p38 MAPK is implicated in regulating ALPase activity in HPCs and may interact with Smad pathway.
本研究旨在探讨p38丝裂原活化蛋白激酶（MAPK）在介导人牙髓细胞（HPCs）碱性磷酸酶（ALPase）活性中的作用。
通过免疫荧光观察转化生长因子β1（TGF-β1）处理的分离HPCs中p38的核转位。使用TGF-β1检测p38 MAPK与Smad信号通路之间的相互作用。用p38信号通路的特异性抑制剂SB203580确定p38激酶在介导ALPase活性中的作用。加入脂多糖（LPS）或TGF-β1以抑制或增加ALPase活性。采用非配对t检验进行统计学分析。
TGF-β1诱导p38的核转位。用SB203580阻断p38信号通路可抑制Smad2/3向细胞核的转位。与溶剂对照组相比，用SB203580处理的细胞中ALPase活性降低（P <.05）。SB203580加剧了LPS对酶活性的抑制作用（P <.05）。在加入TGF-β1之前用SB203580处理也使ALPase活性显著降低（P <.05）。
这些结果表明，p38 MAPK参与调节HPCs中的ALPase活性，并且可能与Smad信号通路相互作用。
