{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Luoreng ZM"],"funding":["key research and development project (talent introduction project) of ningxia hui autonomous region","National Natural Science Foundation of China","the Science and Technology research project of Ningxia Higher Education School"],"pagination":["122"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8447609"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["52(1)"],"pubmed_abstract":["Mastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3' untranslated region (3' UTR) of the NKIRAS2, but not the 3'UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis."],"journal":["Veterinary research"],"pubmed_title":["MiR-125b regulates inflammation in bovine mammary epithelial cells by targeting the NKIRAS2 gene."],"pmcid":["PMC8447609"],"funding_grant_id":["NGY2020007","2019BEB04002","32060749","31960652"],"pubmed_authors":["Wang XP","Luoreng ZM","Wei DW"],"additional_accession":[]},"is_claimable":false,"name":"MiR-125b regulates inflammation in bovine mammary epithelial cells by targeting the NKIRAS2 gene.","description":"Mastitis is a complex inflammatory disease caused by pathogenic infection of mammary tissue in dairy cows. The molecular mechanism behind its occurrence, development, and regulation consists of a multi-gene network including microRNA (miRNA). Until now, there is no report on the role of miR-125b in regulating mastitis in dairy cows. This study found that miR-125b expression is significantly decreased in lipopolysaccharide (LPS)-induced MAC-T bovine mammary epithelial cells. Also, its expression is negatively correlated with the expression of NF-κB inhibitor interacting Ras-like 2 (NKIRAS2) gene. MiR-125b target genes were identified using a double luciferase reporter gene assay, which showed that miR-125b can bind to the 3' untranslated region (3' UTR) of the NKIRAS2, but not the 3'UTR of the TNF-α induced protein 3 (TNFAIP3). In addition, miR-125b overexpression and silencing were used to investigate the role of miR-125b on inflammation in LPS-induced MAC-T. The results demonstrate that a reduction in miR-125b expression in LPS-induced MAC-T cells increases NKIRAS2 expression, which then reduces NF-κB activity, leading to low expression of the inflammatory factors IL-6 and TNF-α. Ultimately, this reduces the inflammatory response in MAC-T cells. These results indicate that miR-125b is a pro-inflammatory regulator and that its silencing can alleviate bovine mastitis. These findings lay a foundation for elucidating the molecular regulation mechanism of cow mastitis.","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2024-11-20T07:34:38.637Z","creation":"2022-02-11T11:07:56.464Z"},"accession":"S-EPMC8447609","cross_references":{"pubmed":["34535180"],"doi":["10.1186/s13567-021-00992-0"]}}