ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2012
FTY720 mediates activation suppression and G(0)/G (1) cell cycle arrest in a concanavalin A-induced mouse lymphocyte pan-activation model.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Early-life fingolimod treatment improves intestinal homeostasis and pancreatic immune tolerance in non-obese diabetic mice.Acta pharmacologica Sinica · 2021Article
- 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.Inflammation · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveFTY720 is a potent drug for multiple sclerosis treatment. To biologically address its possible applications to more generalized diseases with aberrant inflammation, we are testing whether FTY720 can function as a lymphocyte cell cycle blocker and activation suppressor via a concanavalin A (ConA)-mediated mouse lymphocyte pan-activation model.
methodsMouse lymphocytes were obtained from lymph nodes and subjected to ConA and/or FTY720 treatment. Cell viability was assayed by MTT and mitochondrial assays. Early and late activation, cell cycle, proliferation and intracellular Ca(2+) concentration ([Ca(2+)](i)) were analyzed by flow cytometry.
resultsAt concentrations of less than 500 nM, FTY720 significantly down-regulated both CD69 and CD25 expressions of T cells, as well as inhibiting proliferation of activated lymphocytes. In addition, FTY720 blocked the ConA-induced mitogenesis, exhibiting lymphocyte G(0)/G(1) phase cell cycle arrest with significant reduction of cells in S and G(2)/M phases. Meanwhile, a significant decline in [Ca(2+)](i) was observed. The correlation of [Ca(2+)](i) and cell cycle arrest were validated by employing a [Ca(2+)](i) inhibitor SK&F 96365 and testing with and without FTY720 treatment.
conclusionWe 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.