C‐C motif chemokine ligand 23 abolishes ER stress‐ and LPS‐induced reduction in proliferation of bovine endometrial epithelial cells. Issue 4 (24th November 2017)

• Record Type: Journal Article
• Authors: Lim, Whasun; Bae, Hyocheol; Bazer, Fuller W.; Song, Gwonhwa
• Is Part Of: Journal of cellular physiology. Volume 233:Issue 4(2018:Apr.)
• Page Start: 3529
• Page End: 3539
• Publication Date: 2017-11-24
• Subjects: CCL23 -- endometrial epithelial cell -- proliferation -- signal transduction; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.26210
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract : To reduce embryonic losses in domestic animals for economic production of livestock meat and milk, chemokines and their receptors are required for proper implantation and placentation during early pregnancy. In this study, we investigated the effects of C‐C‐motif chemokine ligand 23 (CCL23) on the proliferation of bovine endometrial (BEND) epithelial cells. CCL23 treatment improved BEND cell proliferation by enhancing PCNA and cyclin D1 expression via activation of the PI3K/AKT and MAPK signaling pathways. In addition, a combination of CCL23 and tunicamycin reversed the ER stress‐induced reduction in cell proliferation and the decreased expression of UPR‐mediated signaling proteins, including IRE1α, PERK, and ATF6α. Moreover, it regulated the lipopolysaccharide‐induced inflammation in BEND cells by inhibiting the expression of pro‐inflammatory cytokines ( IL‐6 and IL‐8 ), and by restoring intracellular Ca 2+ levels. These findings demonstrate that CCL23 improves endometrial development and uterine receptivity required for implantation and placentation during early pregnancy. Abstract : In the present study, we identified that treatment of bovine endometrial (BEND) cells with CCL23 enhanced their proliferation with increased PCNA protein expression, and changed the number of cells within cell cycle phase via the PI3K/AKT and MAPK signal transduction pathways. Furthermore, the ER stress‐ and LPS‐induced reduction in cell proliferation was abolished by additional treatment of BEND cells with CCL23. These results provide evidence that CCL23 is essential for improving endometrial development and uterine receptivity required for implantation and placentation.