FTY720 mediates activation suppression and G0/G1 cell cycle arrest in a concanavalin A-induced mouse lymphocyte pan-activation model

Zeng, Xiaofeng; Wang, Tong; Zhu, Changtai; Ye, Yanxia; Song, Bing; Lai, Xinqiang; Zeng, Yaoying

doi:10.1007/s00011-012-0454-6

Cited by 5 publications

(1 citation statement)

References 42 publications

(59 reference statements)

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“…Inflammation is a major concern in the development/pathology of many diseases. T-cell activation is involved in the onset/pathogenesis of several autoimmune diseases, inflammation-related diseases, and transplant rejection (Zeng et al, 2012). During inflammation, levels of many soluble factors like nitric oxide (NO) and select cytokines are often increased (Feghali & Wright, 1997;Sharma et al, 2007), with macrophages being the major source of these agents (Choi et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Emodin inhibits splenocyte proliferation and inflammation by modulating cytokine responses in a mouse model system

Sharma

Tiku

2015

Journal of Immunotoxicology

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Emodin, an anthraquinone derivative, was investigated for potential anti-inflammatory and anti-proliferative effects in vitro. The potential to induce these outcomes was assessed using concanavalin A (ConA)-stimulated mouse splenocytes. Dose-response studies showed that emodin at 100 µM was not cytotoxic to naive cells, and that the same dose caused proliferation to be significantly reduced in ConA-stimulated cells. In addition, emodin significantly reduced ConA-induced nitric oxide (NO) production and the formation/release of TH1 (IL-2, IFNγ, TNFα) and TH17 (IL-6 and IL-17) cell cytokines, but induced those of TH2 (IL-4) and Treg (IL-10) cells. From the results, it is concluded that earlier-reported immunomodulatory effects imparted by emodin may have been attributable, in part, to anti-proliferative effects on lymphocytes, as well as a shift within the TH1/TH2 and TH17/Treg balance (towards TH2 and Treg). These findings, while providing evidence of mechanisms of emodin immunomodulation, are also potentially important for sparking studies that ultimately may result in the potential use of this agent in preventive and/or corrective strategies against autoimmune and other inflammatory diseases.

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Section: Introductionmentioning

confidence: 99%

Emodin inhibits splenocyte proliferation and inflammation by modulating cytokine responses in a mouse model system

Sharma

Tiku

2015

Journal of Immunotoxicology

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Innate Immunity in the CNS – A Focus on the Myeloid Cell

Moore

Durafourt

Antel

2014

Neuroinflammation and CNS Disorders

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FTY720, a Sphingosine-1 Phosphate Receptor Modulator, Improves Liver Fibrosis in a Mouse Model by Impairing the Motility of Bone Marrow-Derived Mesenchymal Stem Cells

Kong

Wang

et al. 2014

Inflammation

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FTY720 is a novel immunosuppressant that modulates sphingosine 1-phosphate (S1P) receptors for the treatment of several diseases. Several hallmarks of liver fibrosis are influenced by S1P, and the interference of S1P signaling by treatment with FTY720 results in beneficial effects in various animal models of fibrosis. However, whether these treatment strategies suppress liver fibrosis progression is incompletely understood. Here, we investigated the effects and mechanisms by which FTY720 improves liver fibrosis in the carbon tetrachloride (CCl4)-induced mouse model. FTY720 treatment significantly attenuated the expression of fibrotic markers in the injured liver of both wild-type and SCID-beige mice. The migration of bone marrow-derived mesenchymal stem cells (BMSCs) to circulation, and subsequently the injured liver, was suppressed by FTY720. Furthermore, in vitro, phosphorylated-FTY720 blocked the migration of BMSCs mediated by S1P. Thus, FTY720 is an effective therapy for liver fibrosis via the suppression of BMSC migration in the CCl4-induced mouse model.

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FTY720 mediates activation suppression and G0/G1 cell cycle arrest in a concanavalin A-induced mouse lymphocyte pan-activation model

Abstract: We demonstrated that FTY720 induces G(0)/G(1) phase cell cycle arrest, resulting in proliferation inhibition upon lymphocyte pan-activation, which may be related to reduction of overall intracellular Ca(2+) load.

Cited by 5 publications

References 42 publications

Emodin inhibits splenocyte proliferation and inflammation by modulating cytokine responses in a mouse model system

Emodin inhibits splenocyte proliferation and inflammation by modulating cytokine responses in a mouse model system

Innate Immunity in the CNS – A Focus on the Myeloid Cell

FTY720, a Sphingosine-1 Phosphate Receptor Modulator, Improves Liver Fibrosis in a Mouse Model by Impairing the Motility of Bone Marrow-Derived Mesenchymal Stem Cells

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