子宫内膜炎
MAPK/ERK通路
下调和上调
生物
脂多糖
子宫
炎症
内分泌学
内科学
信号转导
癌症研究
细胞生物学
医学
免疫学
怀孕
基因
生物化学
遗传学
作者
Zhipeng Huang,Yu Chen,Cheng Yang,Bin Ma,Shuai Guo,Jinxin Zhang,Nuoer Chen,Talha Umar,Baoyi Yin,Ganzhen Deng
标识
DOI:10.1016/j.jri.2022.103751
摘要
Endometritis is a severe postpartum inflammatory disease that puts cows' reproductive health at risk and causes the dairy industry to suffer significant financial losses. The present study aimed to investigate the regulatory role of miR‑26a in LPS‑induced bovine endometrial epithelial cells (bEECs) and the implication for endometritis. Here, we found inflammatory cell infiltration and destruction of endometrial structure in cow uterus, and dramatic increase in myeloperoxidase (MPO) activity and upregulation of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) in endometritis. Meanwhile, miR-26a was down-regulated, but MAP3K8 was increased in the uterine tissue of endometritis. Similarly, the expression of miR-26a was significantly decreased in LPS-stimulated bEECs, while MAP3K8 was risen. In addition, we further verified that MAP3K8 was a target of miR-26a by dual-luciferase reporter assay. Under LPS stress, over-expressing miR-26a markedly decreased MAP3K8 expression levels, along with the reduced expression of inflammatory factors, such as IL-1β, TNF-α and IL-6, whereas this effect was countered by the inhibition of miR-26a. Furthermore, we demonstrated that miR-26a overexpression prevented the MAPK pathway from being activated by targeting MAP3K8. Then we carried out experiments in LPS-stimulated mice uterus to expound that MAP3K8 was essential in endometritis development, which further confirmed the reliability of the above results. In conclusion, overexpression of miR-26a effectively inhibited the expression of MAP3K8 in LPS-induced bEECs and thereby partially suppressed the activation of MAPK signaling pathway. miR-26a and MAP3K8 may be a promising biomarker and therapeutic target for dairy cow endometritis.
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