ArticleJournal of inflammation (London, England)2013
TRPM2 channels are not required for acute airway inflammation in OVA-induced severe allergic asthma in mice.
Article in Journal of inflammation (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- TRPM2 exacerbates airway inflammation by regulating oxidized-CaMKⅡ in allergic asthma.Heliyon · 2024Article
- Endolysosomal Cation Channels and Lung Disease.Cells · 2022Review
- TRPM2 ion channels regulate macrophage polarization and gastric inflammation during Helicobacter pylori infection.Mucosal immunology · 2017Article
- Tsc1 expression by dendritic cells is required to preserve T-cell homeostasis and response.Cell death & disease · 2017Article
- TRP Channels in Respiratory Pathophysiology: the Role of Oxidative, Chemical Irritant and Temperature Stimuli.Current neuropharmacology · 2015Review
- Article
- TRPM2 Channel-Mediated ROS-Sensitive Ca(2+) Signaling Mechanisms in Immune Cells.Frontiers in immunology · 2015Review
- Alterations of the lung methylome in allergic airway hyper-responsiveness.Environmental and molecular mutagenesis · 2014Article
- Adenine Dinucleotide Second Messengers and T-lymphocyte Calcium Signaling.Frontiers in immunology · 2013Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAirway inflammation and asthma have been linked to oxidative stress and the melastatin-related transient receptor potential cation channel, member 2 (TRPM2), which can be activated by reactive oxygen species (ROS), has emerged as a potential therapeutic target for inflammatory diseases.
objectiveUsing TRPM2 deficient (TRPM2-/-) mice, we investigated whether the TRPM2 ion channel, which mediates calcium (Ca2+) influx and lysosomal Ca2+ release, plays a role in the pathophysiology of severe allergic asthma in mouse.
methodsSevere allergic asthma was initiated in wild type (WT) and TRPM2-/- mice by repeated sensitization with ovalbumin (OVA)/aluminum hydroxide on Days 0, 7 and 14, followed by intranasal challenge on Days 21, 22 and 23. Mice were investigated for the presence of airway responsiveness, airway inflammation, production of allergen-specific antibodies, cytokine response and lung pathology.
resultsThe absence of TRPM2 channels has no obvious effect on major etiologic markers of severe allergic asthma in this mouse model. Neither airway resistance nor mucus production are affected in TRPM2-/- mice. TRPM2 channel ablation also does not alter airway inflammation or immunocyte infiltration and does not affect antibody response or cytokine levels.
conclusionsTRPM2 is not required for airway inflammation in OVA-induced severe allergic asthma in mice. Accordingly, TRPM2 might not be a suitable therapeutic target for airway inflammation caused by allergens in humans.
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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.