Latest research on PGE2

Dinoprostone is a naturally occurring prostaglandin E2 (PGE2). It has important effects in labour. It also stimulates osteoblasts to release factors which stimualtes bone resorption by osteoclasts. As a prescription drug it is used as a vaginal suppository, to prepare the cervix for labour and to induce labour.

Latest findings

B cell stimulations were achieved using goat anti-human IgM/G/A F(ab′)2 (Jackson ImmunoResearch) fragments at 1 μg/ml, anti-CD40 (clone S2C6, Macbeth) at 5 μg/ml, or with IL-4 (PeproTech), IL-10, IL-21 (Miltenyi Biotec), PGE2 (Sigma-Aldrich), IL-15 (Miltenyi Biotec), and BAFF (Miltenyi Biotec) (all at 50 ng/ml). [source, 2016]
Furthermore, B cell activation is associated with a broad range of cytokines; therefore, we assessed the ability of IL-4, IL-10, IL-21, PGE2, IL-15, and BAFF to upregulate LLT1. [source, 2016]
Recently, a body of evidence [13–17] has indicated that MSCs produce a variety of cytokines such as Nitric oxide (NO) and PGE2 that display profound immunoregulatory properties by inhibiting the proliferation and function of several major types of immune cells, including natural killer cells, dendritic cells, and both T and B lymphocytes [18–20]. [source, 2016]
Astaxanthin affects not only the COX2 signalling pathway but also multiple cytokines, like Nitric oxide, interleukin 1-β, Prostaglandin E2, C-Reactive Protein (CRP), NF-κB, and TNFα [72]. [source, 2016]
MSCs possess an immunomodulatory role on immune cells including T and B cells by direct cell-to-cell contact-dependent mechanisms [32, 33] and/or the production of soluble factors, such as indoleamine 2,3-deoxigenase [34], Prostaglandin E2 [16–18], NO [11, 35, 36], TGFβ [37], hepatocyte growth factor [37], IL-10 [38], IFNγ [39], and TNFα [15]. [source, 2016]
Moreover, it has been proposed that microglial PGE2 receptor subtype 2 (EP2) signaling contributes to Aβ plaque burden in AD transgenic mice [7, 8], and that EP2 signaling suppresses microglial phagocytosis of Aβ42 in primary microglia cultures [9, 10]. [source, 2016]
Recent evidence suggests that curcumin inhibits the production of microglia-derived PGE2 in response to inflammatory stimulation [17]. [source, 2016]
Given the fact that PGE2 is highly released in the AD brain [5, 6] and has a depressed effect on microglial phagocytosis [7, 8], we hypothesized that curcumin regulates microglial phagocytosis via PGE2 and its related signaling pathway. [source, 2016]
Herein, we first tested whether both exogenous and endogenous PGE2 are involved in immunomodulatory phagocytosis in fAβ42-stimulated N9 microglial cells (N9 cells). [source, 2016]
We then evaluated the ability of curcumin to ameliorate phagocytic abilities of PGE2 and fAβ42-stimulated N9 cells. [source, 2016]