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Persistent endometritis caused by bacterial infections has lethal effects on the reproductive performance of dairy cattle, which compromises animal welfare and delays or prevents pregnancy. The microRNA (miRNA) miR\u201034 family plays a pivotal role in the inflammatory process; however, the precise mechanism of miR\u201034a in endometritis has not been thoroughly elucidated to date. <jats:italic>Methods<\/jats:italic>. In this study, the endometrium of cows diagnosed with endometritis was harvested for bacterial culture and Gram staining to evaluate bacterial contamination of the uterus. Based on this, a bovine endometrial epithelial cell (BEND) inflammation model and a mouse model stimulated with lipopolysaccharide (LPS) <jats:italic>in vitro<\/jats:italic> and <jats:italic>in vivo<\/jats:italic> were constructed. Cell viability was assessed by CCK\u20108, trypan blue staining, and flow cytometry. H&amp;E was applied to histopathological analysis. Immunohistochemical, immunofluorescence, qRT\u2010PCR, and western blot assays were performed to measure the mRNA and protein expression of relevant genes. Online databases, plasmid construction, and dual\u2010luciferase reporter gene assays were used to predict and validate the interaction between miR\u201034a and its target gene LGR4. Finally, mice were injected vaginally with a local antagomir to validate the role of miR\u201034a in murine uterine inflammation. <jats:italic>Results<\/jats:italic>. In this study, we observed that Gram\u2010negative bacteria, represented by <jats:italic>Escherichia coli<\/jats:italic>, are the predominant pathogenic agents responsible for the recurrent occurrence of endometritis in dairy cows. Further, miR\u201034a was found to repress the expression of LGR4 by targeting the 3\u2009<jats:sup>\u2032<\/jats:sup> untranslated region (3\u2009<jats:sup>\u2032<\/jats:sup>UTR) of LGR4. miR\u201034a was upregulated in bovine uterine tissues and bovine endometrial epithelial cells stimulated with LPS. miR\u201034a induced the release of the proinflammatory cytokines IL\u20101<jats:italic>\u03b2<\/jats:italic>, IL\u20106, and TNF\u2010<jats:italic>\u03b1<\/jats:italic> by activating the phosphorylation of NF\u2010<jats:italic>\u03ba<\/jats:italic>B p65. Furthermore, IL\u20101<jats:italic>\u03b2<\/jats:italic> upregulated miR\u201034a transcription and downregulated LGR4 expression in an IL\u20101<jats:italic>\u03b2<\/jats:italic>\u2010dependent manner. <jats:italic>Conclusions<\/jats:italic>. Taken together, our study confirmed that miR\u201034a is regulated by IL\u20101<jats:italic>\u03b2<\/jats:italic> and suppresses the level of the LGR4 3\u2009<jats:sup>\u2032<\/jats:sup>UTR, which in turn exacerbates the inflammatory response. Thus, the knockdown of miR\u201034a might be a new direction for the treatment of endometritis.<\/jats:p>","DOI":"10.1155\/2021\/1744754","type":"journal-article","created":{"date-parts":[[2021,8,29]],"date-time":"2021-08-29T19:05:08Z","timestamp":1630263908000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Enhanced Expression of miR\u201034a Enhances <i>Escherichia coli<\/i> Lipopolysaccharide\u2010Mediated Endometritis by Targeting LGR4 to Activate the NF\u2010<i>\u03ba<\/i>B 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