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Transcriptome analysis reveals the regulation of miR-19b on inflammation in bovine mammary epithelial cells. | LitMetric

Transcriptome analysis reveals the regulation of miR-19b on inflammation in bovine mammary epithelial cells.

Microb Pathog

College of Animal Science and Technology, Ningxia University, Yinchuan 750021, China; Key Laboratory of Ruminant Molecular Cell Breeding, Ningxia Hui Autonomous Region, Yinchuan 750021, China. Electronic address:

Published: December 2024

MicroRNAs (miRNAs) are involved in various biological processes where they regulate the expression of mRNAs. Bovine mammary epithelial cells (bMECs) are functional cells that mediate mammary inflammatory immunity. Although numerous miRNAs regulate the function of bMECs, the role of miR-19b in bMECs has not been reported. In this study, the transcriptome of miR-19b overexpressed bMECs was analyzed by RNA-seq. Additionally, the differentially expressed genes (DEGs) were analyzed to establish the role of miR-19b in bMECs. The results revealed 269 DEGs between the miR-19b overexpression group and the negative control, including 199 up-regulated and 70 down-regulated genes. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that the DEGs regulated immune and inflammatory responses through Staphylococcus aureus (S. aureus) infection and phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway. In addition, the expression of miR-19b was significantly upregulated in lipophosphoric acid (LTA)-induced bMECs, and overexpression of miR-19b negatively regulated the expression of inflammatory cytokines IL-1β and IL-6, thereby alleviating the inflammatory response of LTA-induced bMECs. Based on the above results, we speculate that miR-19b may inhibit in dairy cow mammary inflammation caused by S. aureus, and this process may be mediated through the regulation of relevant gene expression and signaling pathways. The findings from this study provide a new reference for analyzing the molecular regulation of miR-19b in bMECs.

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Source
http://dx.doi.org/10.1016/j.micpath.2024.107082DOI Listing

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