ArticleMediators of inflammation2011
Gene expression profiling in lungs of chronic asthmatic mice treated with galectin-3: downregulation of inflammatory and regulatory genes.
Article in Mediators of inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 24 citations in OpenAlex.
- The Role of Galectins in Asthma Pathophysiology: A Comprehensive Review.Current issues in molecular biology · 2024Review
- Galectin-3, a damage-associated molecular pattern, in tears of patients with vernal keratoconjunctivitis.Japanese journal of ophthalmology · 2023Article
- Development of Galectin-3 Targeting Drugs for Therapeutic Applications in Various Diseases.International journal of molecular sciences · 2023Review
- Article
- Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z.International journal of molecular sciences · 2018Review
- Regulation of Eosinophil Recruitment and Activation by Galectins in Allergic Asthma.Frontiers in medicine · 2017Review
- Galectin-3 Is Associated with Restrictive Lung Disease and Interstitial Lung Abnormalities.American journal of respiratory and critical care medicine · 2016Article
- Allergic asthma biomarkers using systems approaches.Frontiers in genetics · 2014Review
- Galectin-3: its role in asthma and potential as an anti-inflammatory target.Respiratory research · 2013Review
- Reduced expression of galectin-1 and galectin-9 by leucocytes in asthma patients.Clinical and experimental immunology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAsthma is a disorder characterized by a predominance of Th2 cells and eosinophilic inflammation. Suppressors of cytokine signaling (SOCS) proteins act as negative regulators of cytokine signaling. In particular, SOCS1 and SOCS3 play an important role in immune response by controlling the balance between Th1 and Th2 cells. In a previous study, we demonstrated that treatment of chronic asthmatic mice with gene therapy using plasmid encoding galectin-3 (Gal-3) led to an improvement in Th2 allergic inflammation.
methodsUsing a microarray approach, this study endeavored to evaluate the changes produced by therapeutic Gal-3 delivered by gene therapy in a well-characterized mouse model of chronic airway inflammation. Results were confirmed by real-time RT-PCR, Western blot and immunohistochemical analysis.
resultsWe identify a set of genes involved in different pathways whose expression is coordinately decreased/increased in mice treated with Gal-3 gene therapy. We report a correlation between Gal-3 treatment and inhibition of SOCS1 and SOCS3 expression in lungs.
conclusionThese results suggest that negative regulation of SOCS1 and 3 following Gal-3 treatment could be a valuable therapeutic approach in allergic disease.
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.