کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5794427 | 1554304 | 2016 | 8 صفحه PDF | دانلود رایگان |
- PGE2 at certain concentrations exerts a proapoptotic effect on bovine NK cells7.
- Blockade of EP1-4 receptors does not prevent the PGE2-induced apoptosis of NK cells.
- PGE2 at certain concentrations impairs the proliferation of NK cells in cattle.
- Anti-proliferative action of PGE2 on bovine NK cells is mediated via the EP4 receptor
The aim of this research was to determine whether prostaglandin E2 (PGE2) affects bovine NK cells in respect of their counts, apoptosis and proliferation, and if it does, then which of the PGE2 receptor (EP) subtype(s) mediate(s) these effects. We here report that long-term, but not short-term, exposure of bovine peripheral blood mononuclear cells to PGE2 at 10â 5 M, 10â 6 M and 10â 7 M, but not at 10â 8 M, caused a significant increase in the percentage of early apoptotic cells among NK cell subset. Moreover, PGE2 at 10â 5 M and 10â 6 M, but not at 10â 7 M and 10â 8 M, induced a considerable decrease in the absolute count of NK cells. The magnitude of these effects increased with an increasing concentration of PGE2. The blockade of EP1, EP2, EP3 and EP4 receptors did not prevent the PGE2-induced apoptosis and depletion of NK cells. The results suggest that the proapoptotic effect of PGE2 is secondary in character and the induction of this effect is not mediated through EP receptors. Furthermore, the studies demonstrated that PGE2 at 10â 5 M and 10â 6 M, but not at 10â 7 M and 10â 8 M, highly significantly reduced the percentage of proliferating NK cells. The EP1, EP1/2 and EP3 receptor antagonists were unable to block this effect significantly, whereas the selective blockade of EP4 receptors prevented the PGE2-induced inhibition of NK cells proliferation. These results indicate that PGE2 at certain concentrations may impair the proliferation of NK cells and this effect is mediated via the EP4 receptor.
Journal: Research in Veterinary Science - Volume 107, August 2016, Pages 80-87