IFNT-induced IRF1 enhances bovine endometrial receptivity by transactivating LIFR.

Interferon-τ (IFN-τ) participates in the establishment of endometrial receptivity in ruminants. However, the precise mechanisms by which IFN-τ establishes bovine endometrial receptivity remain largely unknown. Interferon regulatory factor 1 (IRF1) is a classical interferon-stimulated gene (ISG) induced by type I interferon, including IFN-τ.

Enhanced expression of miR-26a ameliorates lipopolysaccharide-induced endometritis by targeting MAP3K8 to inactivate MAPK signaling pathway.

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.

microRNA-196b alleviates lipopolysaccharide-induced inflammatory injury by targeting NRAS.

Bovine endometritis is a serious hazard to husbandry, so it is necessary to know the mechanism of endometritis. In past research, we found microRNAs (miRNAs) might be regulators in inflammation, including miR-196b, but the mechanism of miR-196b in bovine endometritis was unknown. Therefore, we tended to find out what role miR-196b would play in bovine endometritis.

MiR-193a-3p targets LGR4 to promote the inflammatory response in endometritis.

Solving the reproductive barriers of dairy cows has become one of the most critical factors determining the dairy industry's development. Clinically, inflammation disease like endometritis is the most crucial cause in reducing dairy production's financial viability. MiR-193 family can induce cell apoptosis and differentiation has been reported in various diseases.

Reduced expression of MiR-125a-5p aggravates LPS-induced experimental acute kidney injury pathology by targeting TRAF6.

Aims: Patients with acute kidney injury (AKI) have higher mortality, and sepsis is among its main causes. MicroRNAs (miRNAs) are essential for regulating kidney function and could have curative potential. This study explored the possibility to treat AKI with miR-125a-5p and reveal the possible mechanism.

MicroRNA-211 regulates the expression of TAB1 and inhibits the NF-κB signaling pathway in lipopolysaccharide-induced endometritis.

Endometritis is a common postpartum inflammatory disease that endangers the reproductive health of humans and animals. Emerging evidence shows that microRNA is a new type of therapeutic molecule that plays a vital role in many diseases; however, its mechanism of action in lipopolysaccharide (LPS)-induced endometritis is still unclear. This study aims to investigate the regulatory role of miR-211 in the innate immune response involved in endometritis, and to evaluate its potential therapeutic value.