Kitamura C, Ogawa Y, Nishihara T, Morotomi T, Terashita M
Department of Operative Dentistry and Endodontics, Kyushu Dental College, 2-6-1 Manazuru, Kokurakita, Kitakyushu 803-8580, Japan.
J Dent Res. 2003 Feb;82(2):91-5. doi: 10.1177/154405910308200203.
The c-Jun N-terminal kinase (JNK) pathway and heat-shock proteins (HSPs) are involved in stress-induced apoptosis. Here we examined the association of JNK, c-Jun, and anti-apoptotic HSPs with pulp apoptosis during wound healing. In normal pulp, c-Jun was activated only in a few pulp cells, but JNK was not. HSP70 was expressed in the cytoplasm of pulp cells. One day after injury, active JNK and c-Jun were detected in apoptotic pulp cells, whereas HSP70 was detected in non-apoptotic cells. We also found the translocation of HSP70 into nuclei of pulp cells, and co-localization with active JNK and c-Jun. Four days after injury, active JNK and c-Jun disappeared in pulp cells, and HSP70 was relocalized from nuclei to the cytoplasm. These results suggest that the JNK pathway may be one of the compartments inducing apoptosis in pulp cells, and that HSP70 may have an inhibitory role in the apoptosis of pulp cells during wound healing.
c-Jun氨基末端激酶（JNK）信号通路和热休克蛋白（HSPs）参与应激诱导的细胞凋亡。在此，我们研究了伤口愈合过程中JNK、c-Jun和抗凋亡HSPs与牙髓细胞凋亡的关系。在正常牙髓中，只有少数牙髓细胞中的c-Jun被激活，但JNK未被激活。HSP70在牙髓细胞的细胞质中表达。损伤一天后，在凋亡的牙髓细胞中检测到活性JNK和c-Jun，而在非凋亡细胞中检测到HSP70。我们还发现HSP70转位至牙髓细胞核内，并与活性JNK和c-Jun共定位。损伤四天后，牙髓细胞中的活性JNK和c-Jun消失，HSP70从细胞核重新定位至细胞质。这些结果表明，JNK信号通路可能是诱导牙髓细胞凋亡的机制之一，并且HSP70在伤口愈合过程中可能对牙髓细胞凋亡具有抑制作用。
