ArticleHeliyon2024
TRPM2 exacerbates airway inflammation by regulating oxidized-CaMKⅡ in allergic asthma.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- Silencing SMAD4 inhibits inflammation and ferroptosis in asthma by blocking the IL-17A signaling pathway.Respiratory research · 2024Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Airway epithelial cells play important roles in allergic asthma. Transient receptor potential melastatin-related 2 (TRPM2) and oxidized Ca Methods: BEAS-2B cells were treated with different dose of IL-13 (0, 5, 10, 20 ng/mL) for 24 h to analyze the changes of TRPM2 and ox-CaMKⅡ protein. Cells expressing different level of TRPM2 were obtained by transfection of TRPM2 siRNA or TRPM2-short cDNA. The transfected cells were treated with 10 ng/mL of IL-13 to analyze the effects of TRPM2 on the ox-CaMKⅡ. A CaMKⅡ inhibitor KN-93 was used to confirm the effects of TRPM2 on levels of ox-CaMKⅡ, Results: Cell viability was clearly decreased by the 20 ng/mL of IL-13. The levels of TRPM2 and ox-CaMKII protein in cells were increased with increasing doses of IL-13. Transfection of TRPM2 siRNA or TRPM2-short cDNA respectively decreased or increased the levels of ox-CaMKⅡ in the IL-13-stimulated cells. The results of KN-93 treatment were similar to the results of TRPM2 siRNA transfection, that the levels of ox-CaMKⅡ, Conclusions: TRPM2 plays a vital role in regulating ox-CaMKⅡ in airway epithelial cells during allergic asthma.
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