Low-dose anisomycin is sufficient to alter the bio-behaviors of Jurkat T cells
| Autor: | Manman Sun, Jingfang Di, Feiyue Xing, Jing Liu, Shan Zeng, Shan Pan |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
QH301-705.5
T cell proliferation Biology anisomycin Jurkat cells General Biochemistry Genetics and Molecular Biology chemistry.chemical_compound medicine IL-2 receptor Biology (General) Anisomycin General Immunology and Microbiology General Neuroscience CD69 apoptosis hemic and immune systems Cell cycle In vitro Cell biology medicine.anatomical_structure chemistry Apoptosis jurkat t cell activation cell cycle General Agricultural and Biological Sciences |
| Zdroj: | Open Life Sciences, Vol 8, Iss 12, Pp 1230-1240 (2013) |
| ISSN: | 2391-5412 |
| Popis: | Anisomycin is a pyrrolidine antibiotic isolated from Streptomyces griseolus. It has been found that a quite low dose of anisomycin is sufficient to block proliferation of primary T lymphocytes. The focus of this study is to explore the possibility of anisomycin to treat human acute leukemia Jurkat T cells in vitro. The results indicated that the low dose of anisomycin could significantly inhibit the colony formation of Jurkat T cells and elevate the inhibition rate of Jurkat T cell growth along with its increasing concentrations. Jurkat T cell cycle was blocked into S-phase by anisomycin. Consistent with the increased proportion of sub-G1 phase, anisomycin promoted Jurkat T cell apoptosis. The CD69 and CD25 expression on the surface of Jurkat T cells was also down-regulated prominently along with the enhancing concentrations of anisomycin, followed by the decreased production of IL-4, IL-10, IL-17, TGF-β and IFN-γ, and the down-regulated expression of phosphorylated-ERK1/2. The results suggest that the suppressive effect of anisomycin on Jurkat T cell growth may be related to inhibiting TGF-β production and ERK1/2 activation, arresting the cell cycle at S-phase and promoting the apoptosis of Jurkat T cells. |
| Databáze: | OpenAIRE |
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