Dual Role of Autophagy in Lipopolysaccharide-induced Preodontoblastic Cells
Dual Role of Autophagy in Lipopolysaccharide-induced Preodontoblastic Cells
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DOI：
10.1177/0022034514553815
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发表时间：
2015-01-01
影响因子：
7.6
通讯作者：
Chen, Z.
中科院分区：
文献类型：
--
作者：
Pei, F.;Lin, H.;Chen, Z.
成牙本质细胞来源于神经嵴来源的牙源性间充质细胞，是宿主重要的防御屏障。成牙本质细胞的存活和免疫功能在保护牙本质-牙髓结构中起重要作用。自噬可以清除受损的细胞器并回收细胞成分以促进细胞内稳态。自噬可以被外部应激激活，如饥饿，缺氧和感染。本研究旨在探讨自噬在炎症成牙本质细胞中的作用及其可能的机制。细胞活力不受轻度脂多糖（LPS）刺激，自噬在此过程中被激活。轻链3的免疫荧光证实LPS处理诱导自噬。早期自噬抑制导致细胞活力下调，与晚期自噬抑制时细胞活力上调相反。Western blot结果显示，p-Akt和survivin在早期没有被激活，后期逐渐增加并达到高峰。晚期自噬通过Akt/mTOR/survivin途径下调。因此，自噬在炎症的成牙本质细胞中具有双重作用，这表明其在维持成牙本质细胞微环境稳态中的重要性。自噬在早期被诱导为一种生存机制，在晚期通过Akt/mTOR/survivin信号通路减少。
Odontoblasts derive from neural crest-derived odontogenic mesenchymal cells, and they are an important barrier of defense for the host. Survival and immunity of odontoblasts play important roles in protecting the dentin-pulp structure. Autophagy can eliminate damaged organelles and recycle cellular components to facilitate cellular homeostasis. Autophagy can be activated with external stressors, such as starvation, hypoxia, and infection. In this study, the role of autophagy in inflamed odontoblasts was explored, and its possible mechanism was investigated. Cell viability was not affected by mild lipopolysaccharide (LPS) stimulation, and autophagy was activated during this process. Immunofluorescence of light chain 3 confirmed that autophagy was induced with LPS treatment. Early-stage autophagy inhibition resulted in down-regulated cell viability, contrary to the up-regulated cell viability at late-stage autophagy inhibition. Western blot suggested that p-Akt and survivin were not activated in the early stage, and they gradually increased and peaked in the late stage. Meanwhile, autophagy was down-regulated through the Akt/mTOR/survivin pathway in the late stage. Thus, autophagy has a dual role in inflamed odontoblasts, which indicates its importance in maintaining the microenvironment homeostasis of odontoblasts. Autophagy was induced as a survival mechanism in the early stage, and it decreased through the Akt/mTOR/survivin signaling pathway in the late stage.