bta-mir-499: Inhibition of bta-mir-499 leads to deregulation of the inflammatory response at the maternal-fetal interface and fetal growth retardation [PMC9334902]. Bta-mir-499, derived from placental exosomes, regulates inflammation locally at the maternal-fetal annex through the inhibition of NK-kB signaling [PMC9334902]. Inhibition of bta-mir-499 results in inflammatory deregulation at the maternal–fetal interface, placental loss, and fetal growth restriction [PMC7432060]. Bta-mir-499 contributes to the regulation of local inflammation at the maternal–fetal interface by inhibiting NF-κB signaling [PMC7432060]. Placental exosome-derived bta-mir-499 inhibits LPS-induced inflammation in cultured bovine endometrial epithelial cells and is associated with bovine pregnancy loss in vivo [PMC10036776]. Bta-mir-499 inhibits NF-κB activation via Lin288/let-7 axis, attenuating inflammatory responses in cattle [PMC7991791]. Placental-derived exosomal bta-mir-499 inhibits NF-kB activation by targeting Lin28B/let7 axis at the maternal-fetal interface in early gestation [PMC10034510]. Bta-mir-499 is significantly enriched in early pregnancy exosomes and decreases LPS-induced expression of proinflammatory cytokines by inhibiting NF-kB signaling [PMC5999645]. Exosome-derived bta-miR-499 regulates Lin28B expression, leading to downregulation of proinflammatory cytokine expression through inhibition of NF-kB activation [PMC5999645]. Exosome-derived bta-miR-499 attenuates proinflammatory cytokine expression by negatively regulating NF-kB p65 activation through a loop involving Lin28B and bta-Let7 miRNAs [PMC5999645]. Placental exosome-derived bta-mir-499 is involved in the regulation of uterine inflammation during early pregnancy [PMC5999645]. Bta-mir-499 expression is increased in tissue exposed to S. aureus in bovine responses [PMC7937231].