Role of Endoplasmic Reticulum Stress in Silica-induced Apoptosis in RAW264.7 Cells.

Yong Bin HU; Xia WU; Xiao Feng Qin; Lei Wang; Pin Hua Pan

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Role of Endoplasmic Reticulum Stress in Silica-induced Apoptosis in RAW264.7 Cells.

Author: Yong Bin HU ^{1
,

2} ; Xia WU ¹ ; Xiao Feng QIN ³ ; Lei WANG ⁴ ; Pin Hua PAN ⁵
Author Information

1. Department of Pathology, Xiangya Basic Medical School, Central South University, Changsha 410013, Hunan, China
2. Department of Pathology, Xiangya Hospital, Central South University, Changsha 410008, 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.
Publication Type:Journal Article
Keywords: Alveolar macrophages; Apoptosis; Endoplasmic reticulum stress; Silica
MeSH: Animals; Apoptosis; drug effects; Butylamines; Cell Survival; drug effects; Endoplasmic Reticulum Stress; physiology; Mice; RAW 264.7 Cells; Silicon Dioxide; toxicity
From: Biomedical and Environmental Sciences 2017;30(8):591-600
CountryChina
Language:English
Abstract:
OBJECTIVEWe investigated the role of endoplasmic reticulum stress (ERS) in silica-induced apoptosis in alveolar macrophages in vitro.
METHODSRAW264.7 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.
RESULTSSilica 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.
CONCLUSIONSilica-induced ERS is involved in the apoptosis of alveolar macrophages.