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Prostaglandin E~2~ inhibits the proliferation of human gingival fibroblasts via the EP~2~ receptor and Epac by Evgeny Weinberg; Ella Zeldich; Max M. Weinreb; Ofer Moses; Carlos Nemcovsky; Miron Weinreb is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract Elevated levels of prostaglandins such as PGE~2~ in inflamed gingiva play a significant role in the tissue destruction caused by periodontitis, partly by targeting local fibroblasts. Only very few studies have shown that PGE~2~ inhibits the proliferation of a gingival fibroblast (GF) cell line, and we expanded this research by using primary human GFs (hGFs) and looking into the mechanisms of the PGE~2~ effect. GFs derived from healthy human gingiva were treated with PGE~2~ and proliferation was assessed by measuring cell number and DNA synthesis and potential signaling pathways were investigated using selective activators or inhibitors. PGE~2~ inhibited the proliferation of hGFs dose‐dependently. The effect was mimicked by forskolin (adenylate cyclase stimulator) and augmented by IBMX (a cAMP‐breakdown inhibitor), pointing to involvement of cAMP. Indeed, PGE~2~ and forskolin induced cAMP generation in these cells. Using selective EP receptor agonists we found that the anti‐proliferative effect of PGE~2~ is mediated via the EP~2~ receptor (which is coupled to adenylate cyclase activation). We also found that the effect of PGE~2~ involved activation of Epac (exchange prot

Who reads Prostaglandin E~2~ inhibits the proliferation of human gingival fibroblasts via the EP~2~ receptor and Epac?

Author

Evgeny Weinberg; Ella Zeldich; Max M. Weinreb; Ofer Moses; Carlos Nemcovsky; Miron Weinreb

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0730-2312)

Published

2009

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)