Effects of sequential exposure to lipopolysaccharide and heat stress on dental pulp cells
Effects of sequential exposure to lipopolysaccharide and heat stress on dental pulp cells
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DOI：
10.1002/jcb.20967
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发表时间：
2006-10-15
影响因子：
4
通讯作者：
Terashita, Masamichi
中科院分区：
文献类型：
--
作者：
Kitamura, Chiaki;Nishihara, Tatsuji;Terashita, Masamichi
在本研究中，我们研究了顺序暴露于细菌脂多糖（LPS）和热应激对牙髓细胞的影响。LPS通过激活p38 MAPK诱导牙髓细胞增殖。在整个热应激过程中，热休克蛋白27在有或无LPS的细胞中均有表达，而在短期热应激时，热休克蛋白27被瞬时磷酸化。在LPS处理的细胞中，短期热应激也诱导了HSF 1的磷酸化。在LIPS处理的细胞中，HSF 1和HSP 27在短期热应激下的立即磷酸化依赖于p38 MAPK的激活而发生。然而，在长期热应激下，HSF 1的激活和HSP 27的诱导独立于p38 MAPK发生。此外，LPS处理的细胞中Akt的完全激活立即被短期热应激诱导，并在整个热应激期间持续。I κ B α在LPS和热应激的连续暴露过程中被诱导和磷酸化。这些结果表明，LPS通过修饰和激活热应激反应分子HSF 1和HSP 27以及细胞存活分子Akt和NF-κ B/I κ B α，对热应激下牙髓细胞的保护和死亡具有独特的作用。
In the present study, we examined the effects of sequential exposure to bacterial lipopolysaccharide (LPS) and heat stress on dental pulp cells. LPS induced the proliferation of pulp cells through the activation of p38 MAPK. HSP27 was expressed in cells with or without LPS during the entire period of heat stress, while transiently phosphorylated by short-term heat stress. In LPS-treated cells, short-term heat stress also induced the phosphorylation of HSF1. The immediate phosphorylation of HSF1 and HSP27 in LIPS-treated cells by short-term heat stress occurred dependent on the activation of p38 MAPK. However, with long-term heat stress, the activation of HSF1 and induction of HSP27 occurred independent of p38 MAPK. Further, full activation of Akt in LPS-treated cells was immediately induced by short-term heat stress and lasted during the entire period of heat stress. I kappa B alpha was induced and phosphorylated throughout sequential exposure to LPS and heat stress. These results suggest that LPS has the unique effects on the cytoprotection and the cell death of pulp cells during heat stress through the modification and the activation of heat stress responsive molecules, HSF1 and HSP27, and cell survival molecules, Akt and NF-kappa B/I kappa B alpha.