ADP receptor P2Y(13) induce apoptosis in pancreatic beta-cells.

Research output: Contribution to journalArticle


Pancreatic beta-cell loss represents a key factor in the pathogenesis of diabetes. Since the influence of purinergic signaling in beta-cell apoptosis has not been much investigated, we examined the role of the ADP receptor P2Y(13) using the pancreatic insulinoma-cell line MIN6c4 as a model system. Real time-PCR revealed high expression of the ADP receptors P2Y(1) and P2Y(13). Adding the ADP analogue, 2MeSADP, to MIN6c4 cells induced calcium influx/mobilization and inhibition of cAMP production by activation of P2Y(1) and P2Y(13), respectively. 2MeSADP reduced cell proliferation and increased Caspase-3 activity; both these effects could be fully reversed by the P2Y(13) receptor antagonist MRS2211. We further discovered that blocking the P2Y(13) receptor results in enhanced ERK1/2, Akt/PKB and CREB phosphorylation mechanisms involved in beta-cell survival. These results indicate that P2Y(13) is a proapoptotic receptor in beta-cells as the P2Y(13) receptor antagonist MRS2211 is able to protect the cells from ADP induced apoptosis.


Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Cell Biology
Original languageEnglish
Pages (from-to)445-453
JournalCellular and Molecular Life Sciences
Publication statusPublished - 2010
Publication categoryResearch

Related research output

Tan, C., 2012, Department of Cardiology, Clinical sciences, Lund University. 85 p.

Research output: ThesisDoctoral Thesis (compilation)

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