Role of Endoplasmic Reticulum Stress in Silica-induced Apoptosis in RAW264.7 Cells |
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Authors: | HU Yong Bin WU Xia QIN Xiao Feng WANG Lei PAN Pin Hua |
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Institution: | 1. Department of Pathology, Xiangya Basic Medical School, Central South University, Changsha 410013, Hunan, China;Department of Pathology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China;2. Department of Pathology, Xiangya Basic Medical School, Central South University, Changsha 410013, Hunan, China;Department of Pathology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China;3. Department of Pathology, Xiangya Basic Medical School, Central South University, Changsha 410013, Hunan, China;4. Department of Pathology, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China;5. Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha 410008, Hunan, China |
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Abstract: | Objective We investigated the role of endoplasmic reticulum stress (ERS) in silica-induced apoptosis in alveolar macrophages in vitro. Methods RAW264.7 cells were incubated with 200 μg/mL silica for different time periods. Cell viability was assayed by the MTT assay. Cell apoptosis was evaluated by DAPI staining, flow cytometry analysis, and Western blot analysis of caspase-3. Morphological changes in the endoplasmic reticulum were observed by transmission electron microscopy. The expression of ERS markers binding protein (BiP) and CCAAT-enhancer-binding protein homologous protein (CHOP) was examined by Western blotting and real-time PCR. As an inhibitor of ERS, 4-phenylbutyric acid (4-PBA) was used in the experiments. Results Silica exposure induced nuclear condensation and caspase-3 expression in RAW264.7 cells. The number of apoptotic cells increased after silica exposure in a time-dependent manner. Silica treatment induced expansion of the endoplasmic reticulum. In addition, the expression of BiP and CHOP increased in silica-stimulated cells. Furthermore, 4-PBA treatment inhibited silica-induced endoplasmic reticulum expansion and the expression of BiP and CHOP. Moreover, 4-PBA treatment attenuated nuclear condensation, reduced apoptotic cells, and downregulated caspase-3 expression in silica-stimulated cells. Conclusion Silica-induced ERS is involved in the apoptosis of alveolar macrophages. |
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Keywords: | Silica Alveolar macrophages Endoplasmic reticulum stress Apoptosis |
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