AUTHOR=Chen Ling , Liu Xiaolin , Li Zhixiong , Wang Jian , Tian Rongfu , Zhang Huilin 

TITLE=Integrated Analysis of Transcriptome mRNA and miRNA Profiles Reveals Self-Protective Mechanism of Bovine MECs Induced by LPS

JOURNAL=Frontiers in Veterinary Science

VOLUME=9

YEAR=2022

URL=https://www.frontiersin.org/journals/veterinary-science/articles/10.3389/fvets.2022.890043

DOI=10.3389/fvets.2022.890043

ISSN=2297-1769

ABSTRACT=<p>Many studies have investigated the molecular crosstalk between mastitis-pathogens and cows by either miRNA or mRNA profiles. Here, we employed both miRNA and mRNA profiles to understand the mechanisms of the response of bovine mammary epithelial cells (bMECs) to lipopolysaccharide (LPS) by RNA-Seq. The total expression level of miRNAs increased while mRNAs reduced after LPS treatment. About 41 differentially expressed mRNAs and 45 differentially expressed miRNAs involved in inflammation were screened out. We found the NFκB-dependent chemokine, <italic>CXCL1, CXCL3, CXCL6, IL8</italic>, and <italic>CX3CL1</italic> to be strongly induced. The anti-apoptosis was active because <italic>BCL2A1</italic> and <italic>BIRC3</italic> significantly increased with a higher expression. The effects of anti-microbe and inflammation were weakly activated because <italic>TNF, IL1, CCL20, CFB, S100A, MMP9</italic>, and <italic>NOS2A</italic> significantly increased but with a low expression, <italic>IL6</italic> and β<italic>-defensin</italic> decreased. These activities were supervised by the <italic>NFKBIA</italic> to avoid excessive damage to bMECs. The <italic>bta-let-7a-5p, bta-miR-30a-5p, bta-miR-125b</italic>, and <italic>bta-miR-100</italic> were essential to regulate infection process in bMECs after LPS induction. Moreover, the lactation potential of bMECs was undermined due to significantly downregulated <italic>SOSTDC1, WNT7B, MSX1</italic>, and <italic>bta-miR-2425-5p</italic>. In summary, bMECs may not be good at going head-to-head with the pathogens; they seem to be mainly charged with sending out signals for help and anti-apoptosis for maintaining lives after LPS induction.</p>