Carbon black nanoparticles induce HDAC6-mediated inflammatory responses in 16HBE cells
| Autor: | Hui Lin, Yao Zuo, Guoqing Fu, Yingying Gu, Zhenyu Wang, Lingzhi Qin, Qimei Yu, Ling Zhang, Ting Zhou, Yuqin Shi |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Adult
Male Health Toxicology and Mutagenesis Histone Deacetylase 6 Toxicology Proinflammatory cytokine 03 medical and health sciences 0302 clinical medicine Soot Western blot Downregulation and upregulation Occupational Exposure medicine Humans RNA Messenger Disease Resistance 030304 developmental biology 0303 health sciences Messenger RNA medicine.diagnostic_test Chemistry Public Health Environmental and Occupational Health Interleukin Bronchial Diseases Epithelial Cells Pneumonia Transfection Middle Aged Molecular biology Occupational Diseases 030220 oncology & carcinogenesis Nanoparticles Female Tumor necrosis factor alpha Intracellular |
| Zdroj: | Toxicology and Industrial Health. 36:759-768 |
| ISSN: | 1477-0393 0748-2337 |
| DOI: | 10.1177/0748233720947214 |
| Popis: | Long-term inhalation of carbon black nanoparticles (CBNPs) leads to pulmonary inflammatory diseases. Histone deacetylase 6 (HDAC6) has been identified as an important regulator in the development of inflammatory disorders. However, the direct involvement of HDAC6 in CBNPs-induced pulmonary inflammatory responses remains unclear. To explore whether HDAC6 participates in CBNPs-induced pulmonary inflammation, human bronchial epithelial cell line (16HBE cells) was transfected with HDAC6 small interference RNA (siRNA) and then exposed to CBNPs at concentrations of 0, 25, and 50 µg/ml for 24 h. Intracellular HDAC6 and intraflagellar transport protein 88 (IFT88) mRNA and protein were determined by real-time polymerase chain reaction and Western blot, respectively. The secretions of inflammatory cytokines including interleukin (IL)-8, tumor necrosis factor (TNF)-α, IL-6, and IL-1β were measured by enzyme-linked immunosorbent assay. CBNPs induced a significant increase in the expressions of IL-8 and IL-6, accompanied by a high level of intracellular HDAC6 mRNA when compared with a blank control group ( p < 0.05). However, there were no significant changes in the levels of TNF-α secretion, intracellular HDAC6 and IFT88 protein induced by CBNPs ( p > 0.05). The HDAC6 mRNA expression was significantly suppressed in HDAC6 siRNA-transfected cells ( p < 0.05). The secretions of IL-8, TNF-α, and IL-6 were significantly less in HDAC6 siRNA-transfected cells than that in normal 16HBE cells with exposure to 25 or 50 µg/ml of CBNPs, but intracellular IFT88 mRNA expression was markedly increased in HDAC6 siRNA-transfected cells when compared with normal 16HBE cells exposed to 50 µg/ml of CBNPs (all p < 0.05). Downregulation of the HDAC6 gene inhibits CBNPs-induced inflammatory responses in bronchial epithelial cells, partially through regulating IFT88 expression. It is suggested that CBNPs may trigger inflammatory responses in bronchial epithelial cells by an HDAC6/IFT88-dependent pathway. |
| Databáze: | OpenAIRE |
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