ArticlePurinergic signalling2026
Extracellular ATP induces the proinflammatory phenotype transition of MH7A cells by activating P2X7 receptor.
Article in Purinergic signalling, 2026. 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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Who cites it
1 citing paper in PubMed.
- Damage-Associated Molecular Patterns in Mesothelioma: Drivers of Inflammation and Therapeutic Targets.International journal of molecular sciences · 2026Review
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4 authors.
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Abstract
The transition of fibroblast-like synoviocytes (FLS) toward a proinflammatory phenotype is a hallmark of rheumatoid arthritis (RA), with proinflammatory RA-FLS exacerbating joint destruction via hyperproliferation, enhanced migration/invasion, and excessive inflammatory cytokine secretion. Extracellular ATP (eATP), a key damage-associated molecular pattern, is elevated in RA's inflammatory microenvironment and exerts proinflammatory effects on immune cells via P2X7 receptors (P2X7R), but its role in regulating RA-FLS' proinflammatory phenotype via P2X7R remains unclear. Using MH7A cells (a RA-FLS line), this study investigated eATP's effect on RA-FLS' proinflammatory transition and P2X7R's mediatory role to support FLS-targeted RA therapies. Methods included CCK-8 assays for optimal eATP/antagonist concentrations and metabolic activity, TranswellPlease check if the affiliations are captured correctly. assays for migration/invasion, q-PCR/Western blotting for P2X7R expression, ELISA for IL-1β/IL-6/TNF-α secretion, and Western blotting for NLRP3 (NOD-like receptor protein 3) inflammasome (NLRP3, pro-caspase-1, cleaved-caspase-1) activation. Results showed eATP enhanced MH7A migration/invasion, upregulated P2X7R, increased NLRP3 inflammasome activation, and elevated cytokine secretion, while P2X7R antagonist pretreatment abrogated these changes. Thus, eATP induces MH7A's proinflammatory transition by activating P2X7R, with targeting the eATP-P2X7R pathway representing a promising RA therapeutic target.
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