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首页> 外文期刊>Journal of Cellular Physiology >C‐C motif chemokine ligand 23 abolishes ER stress‐ and LPS‐induced reduction in proliferation of bovine endometrial epithelial cells
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C‐C motif chemokine ligand 23 abolishes ER stress‐ and LPS‐induced reduction in proliferation of bovine endometrial epithelial cells

机译:C量C主题趋化因子配体23废除ER应激所致和LPS诱导减少扩散牛子宫内膜上皮细胞

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摘要

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.
机译:减少在家畜胚胎损失经济生产的牲畜的肉和牛奶,趋化因子及其受体所必需的适当的植入和胎座在早期怀孕。C量C量的影响主题趋化因子配体23 (CCL23)牛子宫内膜的增殖(弯曲)上皮细胞。增殖细胞核抗原、细胞周期蛋白促进细胞增殖D1通过PI3K / AKT激活和表达MAPK信号通路。CCL23和衣霉素逆转ER应激诱导细胞增殖减少和减少的表达UPR的介导信号蛋白,包括IRE1α、活跃ATF6α。脂多糖诱导炎症弯曲通过抑制细胞的表达箴量炎性细胞因子(IL 6和IL 8)应承担的通过恢复细胞内Ca 2 +水平。结果表明CCL23改善子宫内膜发育和子宫接受所需植入和胎座怀孕早期。

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