The role of the globular heads of the C1q receptor in TcdA-induced human colonic epithelial cell apoptosis via a mitochondria-dependent pathway
Autor: | Yongzhong Ning, Yanmin Xu, Lingjuan Gao, Shu Li, Jinhua Liang, Ling Chen, Qi Li, Xiufeng Ma, Li Dong, Heran Yang |
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Rok vydání: | 2020 |
Předmět: |
Microbiology (medical)
Colon Bacterial Toxins lcsh:QR1-502 Clostridium difficile toxin A Apoptosis Mitochondrion Biology TcdA Microbiology lcsh:Microbiology Cell Line Flow cytometry Enterotoxins 03 medical and health sciences Adenosine Triphosphate medicine Humans Gene Silencing Viability assay Mitochondrial function apoptosis Membrane Potential Mitochondrial chemistry.chemical_classification 0303 health sciences Reactive oxygen species Membrane Glycoproteins TUNEL assay medicine.diagnostic_test 030306 microbiology Epithelial Cells Clostridium difficile Molecular biology Mitochondria Receptors Complement Gene Expression Regulation chemistry gC1qR Reactive Oxygen Species Intracellular Research Article |
Zdroj: | BMC Microbiology, Vol 20, Iss 1, Pp 1-12 (2020) BMC Microbiology |
ISSN: | 1471-2180 |
DOI: | 10.1186/s12866-020-01958-6 |
Popis: | Background Clostridioides (formerly Clostridium) difficile infection is the leading cause of antibiotic-associated colitis. Studies have demonstrated that C. difficile toxin A (TcdA) can cause apoptosis of many human cell types. The purpose of this study was to investigate the relationships among exposure to TcdA, the role of the receptor for the globular heads of C1q (gC1qR) gene and the underlying intracellular apoptotic mechanism in human colonic epithelial cells (NCM 460). In this study, gC1qR expression was examined using real-time polymerase chain reaction (PCR), western blotting and immunohistochemical staining. Cell viability was assessed by the water-soluble tetrazolium salt (WST-1) assay, and cell apoptosis was assessed by flow cytometry and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay. Mitochondrial function was assessed based on reactive oxygen species (ROS) generation, changes in the mitochondrial membrane potential (ΔΨm) and the content of ATP. Results Our study demonstrated that increasing the concentration of TcdA from 10 ng/ml to 20 ng/ml inhibited cell viability and induced cell apoptosis (p Conclusion These data support a mechanism by which gC1qR plays a crucial role in TcdA-induced apoptosis of human colonic epithelial cells in a mitochondria-dependent manner. |
Databáze: | OpenAIRE |
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