Anisomycin - Explore the Science & Experts | ideXlab

Scan Science and Technology

Contact Leading Edge Experts & Companies

Anisomycin

The Experts below are selected from a list of 5895 Experts worldwide ranked by ideXlab platform

Anisomycin – Free Register to Access Experts & Abstracts

Feiyue Xing – One of the best experts on this subject based on the ideXlab platform.

  • microrna let 7c is essential for the Anisomycin elicited apoptosis in jurkat t cells by linking jnk1 2 to ap 1 stat1 stat3 signaling
    Scientific Reports, 2016
    Co-Authors: Zhiwei Zhou, Jing Liu, Jin Wang, Jia Xiao, Feiyue Xing

    Abstract:

    Anisomycin, an antibiotic produced by Streptomyces griseolus, strongly induces apoptosis in various tumor cells in vitro, superior dramatically to adriamycin. The present study aims to elucidate its detailed mechanistic process. The results showed that Anisomycin sufficiently promoted the apoptosis in human leukemic Jurkat T cells at a quite low dose. microRNA let-7c (let-7c) contributed to the Anisomycin-induced apoptosis, which could be abrogated by the inactivation of JNK signaling. The let-7c over-expression and the addition of its mimics facilitated the activation of AP-1, STAT1 and Bim by linking JNK1/2 to AP-1/STAT1, but rather inhibited the activation of STAT3 and Bcl-xL by connecting JNK1/2 to STAT3, followed by the augmented apoptosis in the cells. The let-7c deficiency reduced the AP-1, STAT1 and Bim activities, and enhanced the STAT3 and Bcl-xL, alleviating the Anisomycin-induced apoptosis. The knockdown of the bim gene repressed the Anisomycin-boosted apoptosis through the attenuation of the active Bak and Bax. The findings indicate for the first time that miR let-7c is essential for the Anisomycin-triggered apoptosis by linking JNK1/2 to AP-1/STAT1/STAT3/Bim/Bcl-xL/Bax/Bak signaling. This provides a novel insight into the mechanism by which Anisomycin leads to the tumor cell apoptosis, potentially laying the foundations for its development and clinical application.

  • Low-dose Anisomycin is sufficient to alter the bio-behaviors of Jurkat T cells
    Open Life Sciences, 2013
    Co-Authors: Manman Sun, Feiyue Xing, Shan Zeng, Shan Pan, Jing Liu

    Abstract:

    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.

  • In vitro and in vivo evaluation of Anisomycin against Ehrlich ascites carcinoma
    Oncology Reports, 2013
    Co-Authors: Pengtao You, Feiyue Xing, Shan Zeng, Jie Huo, Baoyu Wang, Jing Liu

    Abstract:

    Anisomycin eminently inhibits cell proliferation in vitro. The aim of this study was to explore the potential of Anisomycin to treat tumors in vivo and its mechanism(s) of action. The results showed that peritumoral administration of Anisomycin significantly suppressed Ehrlich ascites carcinoma (EAC) growth resulting in the survival of approximately 60% of the mice 90 days after EAC inoculation. Enhancement of infiltrating lymphocytes was noted in the tumor tissue, which was dramatically superior to adriamycin. The growth inhibitory rate of EAC cells was enhanced with increasing concentrations of Anisomycin, following an enhanced apoptotic rate. The total apoptotic rate induced by 160 ng/ml of Anisomycin was higher when compared to that induced by 500 ng/ml of adriamycin. DNA breakage and nanostructure changes were also noted in the EAC cells. The levels of caspase-3 mRNA, caspase-3 and cleaved-caspase-3 proteins in the Anisomycin‑treated EAC cells were augmented in a dose- and time-dependent manner, following the activation of caspase-8 and caspase-9, which finally triggered PARP cleavage. The cleaved-caspase-3, cleaved-caspase-8 and cleaved-caspase-9 proteins were mainly localized in the nuclei of the cells. These results indicate that Anisomycin efficaciously represses in vitro and in vivo growth of EAC cells through caspase signaling, significantly superior to the effects of adriamycin. This suggests the potential of Anisomycin for the treatment of breast cancer.

Tai-liang Guo – One of the best experts on this subject based on the ideXlab platform.

  • disruption of nox2 and tnfrp55 p75 eliminates cardioprotection induced by Anisomycin
    American Journal of Physiology-heart and Circulatory Physiology, 2012
    Co-Authors: Ting C Zhao, Ling Zhang, Jun T. Liu, Tai-liang Guo

    Abstract:

    Transient activation of p38 through Anisomycin is demonstrated to precondition the heart against myocardial injury. However, it remains unknown whether specific TNF-α receptor (TNFR) p55/p75 and Nox2, a subunit of NADPH oxidase, are involved in this event. We sought to investigate whether the genetic disruption of TNFRp55/p75 and Nox2 eliminated cardioprotection elicited by Anisomycin and whether p38-dependent activation of Nox2 stimulated TNFR to ultimately achieve protective effects. Adult wild-type and TNFR p55/p75−/− and Nox2−/− mice received intraperitoneal injections of Anisomycin (0.1 mg/kg), a potent activator of p38. The hearts were subjected to 30 min myocardial ischemia/30 min reperfusion in the Langendorff perfused heart after 24 h. Left ventricular function was measured, and infarct size was determined. Myocardial TNF-α protein, Nox2, and superoxides releases were detected. Gel kinase assay was employed to detect the effect of p38 on Nox2 phosphorylation. Activation of p38 through Anisomycin produces marked improvements in left ventricular functional recovery, and the reduction of myocardial infarction, which were abrogated by disruption of Nox2 and TNFR p55/p75. Disruption of Nox2 and TNFR p55/p75 abolished the effect of Anisomycin-induced reduction of infarct size. Anisomycin induced the production of TNF-α, which was abrogated in Nox2−/− mice and by treatment with SB203580, but not by disruption of p55/p75. Anisomycin treatment resulted in an increase in Nox2 protein and the phosphorylation of Nox2, which was blocked by inhibition of p38. Taken together, these results indicate that stimulation of the Nox2 and TNFR p55/p75 pathway is a novel approach to Anisomycin-induced cardioprotection.

  • Disruption of Nox2 and TNFRp55/p75 eliminates cardioprotection induced by Anisomycin
    American Journal of Physiology-Heart and Circulatory Physiology, 2012
    Co-Authors: Ting C Zhao, Ling Zhang, Jun T. Liu, Tai-liang Guo

    Abstract:

    Transient activation of p38 through Anisomycin is demonstrated to precondition the heart against myocardial injury. However, it remains unknown whether specific TNF-α receptor (TNFR) p55/p75 and Nox2, a subunit of NADPH oxidase, are involved in this event. We sought to investigate whether the genetic disruption of TNFRp55/p75 and Nox2 eliminated cardioprotection elicited by Anisomycin and whether p38-dependent activation of Nox2 stimulated TNFR to ultimately achieve protective effects. Adult wild-type and TNFR p55/p75−/− and Nox2−/− mice received intraperitoneal injections of Anisomycin (0.1 mg/kg), a potent activator of p38. The hearts were subjected to 30 min myocardial ischemia/30 min reperfusion in the Langendorff perfused heart after 24 h. Left ventricular function was measured, and infarct size was determined. Myocardial TNF-α protein, Nox2, and superoxides releases were detected. Gel kinase assay was employed to detect the effect of p38 on Nox2 phosphorylation. Activation of p38 through Anisomycin produces marked improvements in left ventricular functional recovery, and the reduction of myocardial infarction, which were abrogated by disruption of Nox2 and TNFR p55/p75. Disruption of Nox2 and TNFR p55/p75 abolished the effect of Anisomycin-induced reduction of infarct size. Anisomycin induced the production of TNF-α, which was abrogated in Nox2−/− mice and by treatment with SB203580, but not by disruption of p55/p75. Anisomycin treatment resulted in an increase in Nox2 protein and the phosphorylation of Nox2, which was blocked by inhibition of p38. Taken together, these results indicate that stimulation of the Nox2 and TNFR p55/p75 pathway is a novel approach to Anisomycin-induced cardioprotection.

  • Abstract 146: Disruption of Nox2 and TNFRp55/p75 Eliminates Anisomycin-Induced Preconditioning Effect in the Heart
    Circulation Research, 2012
    Co-Authors: Ting C Zhao, Ling Zhang, Tai-liang Guo

    Abstract:

    Background: Transient activation of p38 through Anisomycin is demonstrated to precondition the heart against myocardial injury. However, it remains unknown whether specific TNF-α receptor (TNFR) p55/p75 and Nox2, a subunit of NADPH-oxidase are involved in this event. Objective: We sought to investigate whether the genetic disruption of TNFRp55/p75 and Nox2 eliminates cardioprotection elicited by Anisomycin and whether p38-dependent activation of Nox2 stimulates TNFR to ultimately achieve protective effects. Methods: Adult wild type and p55/p75 -/- and Nox2 -/- mice received intraperitoneal injections of Anisomycin (0.1mg/kg), a potent activator of p38. The hearts were subjected to 30 min myocardial ischemia /30 min reperfusion in the Langendorff perused heart after twenty four hours. Left ventricular function was measured and infarct size was determined by triphenyltetrazolium chloride. Myocardial TNF-α protein, Nox2 and superoxides releases were detected. Gel kinase assay was employed to detect the effect of p38 on Nox2 phosphorylation. Results: Activation of p38 through Anisomycin produces marked improvements in the recovery of left ventricular end diastolic pressure, rate pressure products, and the reduction of myocardial infarction, which were completely abrogated by disruption of Nox2 and TNFR p55/p75. Genetic disruption of Nox2 and TNFR p55/p75 abolished the effect of Anisomycin-induced reduction of infarct size. Ansiomycin induced the production of TNFα, which was abrogated in Nox2 -/- mice. Notably, activation of p38 resulted in the phosphorylation of Nox2. Conclusion: Taken together, these results indicate that stimulation of the Nox2 and TNFR p55/p75 pathway is a novel approach to Anisomycin-induced cardioprotection.

Wenting Hao – One of the best experts on this subject based on the ideXlab platform.

  • Anisomycin inhibits the behaviors of t cells and the allogeneic skin transplantation in mice
    Journal of Immunotherapy, 2008
    Co-Authors: Feiyue Xing, Jing Liu, Shan Zeng, Di Chen, Ling Chen, Zhiyuan Fang, Zhongfeng Guo, Shan Pan, Jiongkun Wang, Wenting Hao

    Abstract:

    There is still a lack of a high potent and low toxic immunosuppressive drug. We accidentally found that a quite low dose of Anisomycin was sufficient to block proliferation of T cells. In this study, carboxy-fluorescein diacetate-succinimidyl ester staining showed that over 10.0 ng/mL of Anisomycin markedly inhibited the proliferation of T cells induced by ConA. Propidium iodide staining revealed that Anisomycin led to G0/G1 arrest and blocked S phase entry stimulated by ConA or phorbol 12, 13-dibutyrate plus ionomycin. Anisomycin down-regulated remarkably the CD69 and CD25 expression on the surface of T cells. The response of T cells was repressed by treatment of Anisomycin, which was partly restored by adding exogenous interleukin-2, and there was no difference between Anisomycin and dexamethasone, although the used dose of the latter was 100-fold of the former. The inhibition of cytotoxicity of T cells against 7919 cells by Anisomycin was observed without the direct cytotoxicity to T cells or 7919 cells. The level of transforming growth factor-beta1 fell by <80.0 ng/mL in vitro and 30.0 mg/kg of Anisomycin in vivo and enhanced by more than the doses. The treatment of Anisomycin prolonged the survival of the transplanted skin and depressed the delayed type hypersensitivity development and the T-cell response in the skin-transplanted mice. Moreover, the effect of its restraining allograft rejection might be superior to cyclosporine A, with relatively slight toxic signs. These results indicate Anisomycin significantly inhibits the behaviors of T cells and the transplantation rejection, providing important evidence for Anisomycin as a novel immunosuppressant.