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PTGFR activation promotes the expression of PTGS-2 and growth factors via activation of the PKC signaling pathway in bovine endometrial epithelial cells

Gao, Long, Gao, Ruifeng, Mao, Wei, Liu, Bo, Zhang, Shuangyi, Tahala, Duri, Fu, Changqi, Shen, Yuan, Wu, Jindi, Deng, Yang, Li, Qianru, Cao, Jinshan
Animal reproduction science 2018 v.199 pp. 30-39
agonists, antagonists, cattle, endometrium, epithelial cells, gene expression, gene expression regulation, interleukin-8, messenger RNA, phosphorylation, prostaglandin synthase, prostaglandins, protein kinase C, proteins, signal transduction, transforming growth factor beta 1, vascular endothelial growth factors
The endometrium of domestic animals has a remarkable capacity to self-repair. Prostaglandin F2α (PGF2α) is one of the major prostaglandins secreted from the endometrium. The role of PGF2α in endometrial repair, however, is still unknown. In the present study, it was investigated whether prostaglandin F2α receptor (PTGFR) activation could induce expression of prostaglandin-endoperoxide synthase 2 (PTGS-2) and growth factors associated with endometrial repair via activation of protein kinase C (PKC) signaling in endometrial epithelial cells (bEECs) of cattle. Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-β1), and interleukin-8 (IL-8). The increased abundances of these proteins were suppressed by the treatment with the PTGFR antagonist, AL8810.Furthermore, fluprostenol treatment also induced PKC phosphorylation. Subsequently, treatment with AL8810 inhibited the fluprostenol-induced PKC phosphorylation. Additionally, treatment with the PKC inhibitor, chelerythrine, reduced the fluprostenol-induced increase in the relative abundance of VEGF, CTGF, TGF-β1, and IL-8 mRNA in bEECs. Taken together, these results suggest that PTGFR activation may induce endometrial repair by upregulating PTGS-2 gene expression and stimulating VEGF, CTGF, TGF-β1, and IL-8 gene expression via activation of the PKC signaling pathway.