ArticleJournal of clinical & cellular immunology2011
Transforming Growth Factor-
Article in Journal of clinical & cellular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- RNA Seq profiling reveals a novel expression pattern of TGF-β target genes in human blood eosinophils.Immunology letters · 2015Article
- Determinants of eosinophil survival and apoptotic cell death.Apoptosis : an international journal on programmed cell death · 2015Review
- Regulation of spontaneous eosinophil apoptosis-a neglected area of importance.Journal of cell death · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEosinophils rapidly undergo apoptosis unless exposed to prosurvival cytokines such as interleukin 5 (IL-5) or granulocyte-macrophage colony stimulating factor (GM-CSF).
objectiveThe objective of this study was to investigate the proapoptotic effects of TGF-β alone and in combination with IL-5 on eosinophils.
methodsPeripheral blood eosinophil (PBEos) viability was assessed using flow cytometry after exposure to TGF-β1 and IL-5. Calpain-1 activation was determined in cell extracts by western blot analysis of endogenous substrates and with a fluorogenic α-spectrin substrate. Molecular interactions between calpain1 and calpastatin were assessed by immunoprecipitation and western blotting.
resultsPhysiologic concentrations of TGF-β1 significantly antagonized the prosurvival effects of IL-5. TGF-β1-induced apoptosis was suppressed by inhibitors of calpain, or its downstream target, caspase 3. TGF-β1 signaling through Smad3 was unaffected by IL-5 and was required for the pro-apoptotic effects of TGF-β1. However, IL-5 induced Akt phosphorylation was inhibited by TGF-β1 and was associated with accelerated calpain cleavage and eosinophil death.
conclusionTGF-β1 induces calpain-1 activation through antagonism of Akt which induces caspase activation and eosinophil apoptosis.
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.