ArticleBritish journal of pharmacology2013
UDP induces intestinal epithelial migration via the P2Y6 receptor.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- High-fat diet-derived metabolite uridine diphosphate (UDP) impairs epithelial regeneration by P2YGut microbes · 2026Article
- Inhibition of (interstitial) P2YPflugers Archiv : European journal of physiology · 2026Article
- Inhibition of (interstitial) P2YResearch square · 2026Article
- Inhibition of (interstitial) P2YbioRxiv : the preprint server for biology · 2026Article
- P2YJournal of immunology research · 2026Article
- Nucleotide metabolism in cancer cells fuels a UDP-driven macrophage cross-talk, promoting immunosuppression and immunotherapy resistance.Nature cancer · 2024Article
- P2YFrontiers in pharmacology · 2018Article
- Article
- Anti-proliferative Effects of Nucleotides on Gastric Cancer via a Novel P2Y6/SOCE/CaScientific reports · 2017Article
- Thymidine 5'-O-monophosphorothioate induces HeLa cell migration by activation of the P2Y6 receptor.Purinergic signalling · 2016Article
- Purinergic signalling in the gastrointestinal tract and related organs in health and disease.Purinergic signalling · 2014Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeExtracellular nucleotides are released at high concentrations from damaged cells and function through P2 receptor activation. Intestinal epithelial restitution, which is defined as cell migration independent of cell proliferation, is an important initial step in the process of wound healing. In this study, we investigated the role of extracellular nucleotides in intestinal epithelial migratory responses. EXPERIMENTAL APPROACH: Wound-healing and trans-well migration assays were performed with a rat intestinal epithelial cell line (IEC-6). The concentrations of extracellular nucleotides released from injured IEC-6 cells were measured by HPLC. TGF-β expression was assessed by RT-PCR and elisa. KEY
resultsScratching the monolayer of IEC-6 cells induced cell migration. Pretreatment with apyrase or MRS2578, a selective P2Y6 antagonist, inhibited the wound-induced cell migration. Among the cellular nucleotides, only ATP and uridine 5'-diphosphate (UDP) were detected in the culture medium after cell wounding. Exogenously applied UDP dose-dependently enhanced the migration more effectively than ATP but did not induce proliferation. In addition, cell wounding and UDP increased the expression of TGF-β, and both the wound-induced and UDP-enhanced migration were inhibited by MRS2578 or ALK5Inhibitor (ALK5i), a TGF-β receptor blocker. Furthermore, cell wounding and UDP stimulation up-regulated the expression of P2Y6 receptor mRNA, and this effect was suppressed by MRS2578 or ALK5i. CONCLUSION AND IMPLICATIONS: Wound-induced UDP evokes intestinal epithelial restitution by activation of P2Y6 receptors, which mediates de novo synthesis of TGF-β. In addition, the expression of P2Y6 receptors is increased by cell wounding and UDP, which constitutes a positive-feedback loop for mucosal repair.
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