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Published on: September 4, 2012
Long non-coding RNA (CMR) involved in autoprotection in S. aureus mastitis in dairy cows by regulating miR-877/FOXM1
Shuangfeng Chu1, Tianqi Zhao1, Mingxun Li1
1College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China; Joint International Research Laboratory of Agriculture & Agri-Product Safety, Ministry of Education, Yangzhou University, Yangzhou 225009, China.
Abstract:
Long non-coding RNAs (LncRNAs) are dysregulated in a variety of human diseases and are highly involved in the development and progression of tumors. Studies on lncRNAs associated with cow mastitis have been lagging behind compared to humans or model animals, therefore, the aim of this study was to explore the mechanism of LncRNAs (CMR) involved in autoprotection against S. aureus mastitis in Bovine Mammary Epithelial Cells (BMECs). First, qRT-PCR was used to examine the relative expression of CMR in a S. aureus mastitis model of BMECs. Then, cell proliferation and apoptosis were detected by EdU and apoptosis assay. Finally, the targeting relationship between miRNAs and mRNA/LncRNAs was determined by dual luciferase reporter gene, qRT-PCR and western blotting techniques. The results showed that CMR was upregulated in the S. aureus mastitis model of BMECs and promoted the expression of inflammatory factors, and SiRNA-mediated CMR inhibited the proliferation of mammary epithelial cells and induced apoptosis. Mechanistically, CMR acts as a competitive endogenous RNA (ceRNA) sponge miR-877, leading to upregulation of FOXM1, a target of miR-877. Importantly, either miR-877 overexpression or FOXM1 inhibition abrogated CMR knockdown-induced apoptosis promoting cell proliferation and reducing inflammatory factor expression levels. In summary, CMR is involved in the regulation of autoprotection against S. aureus mastitis through the miR-877/FOXM1 axis in BMECs and induces immune responses in mammary tissues and cells of dairy cows, providing an important reference for subsequent prevention and control of cow mastitis and the development of targeted drugs.
Insights
Long non-coding RNA (LncRNA) CMR promotes S. aureus mastitis in cows by regulating the miR-877/FOXM1 pathway. Inhibiting CMR boosts cow mammary cell immunity and reduces inflammation, offering new therapeutic targets for mastitis.
Area of Science:
- Veterinary immunology
- Molecular biology
- Dairy science
Background:
- Long non-coding RNAs (LncRNAs) are implicated in human diseases, but their role in bovine mastitis is understudied.
- Cow mastitis, caused by S. aureus, significantly impacts dairy production and animal welfare.
Purpose of the Study:
- To investigate the mechanism of a specific LncRNA (CMR) in bovine mammary epithelial cells (BMECs) during S. aureus mastitis.
- To elucidate the regulatory pathway involving LncRNAs, microRNAs, and mRNAs in cow mastitis autoprotection.
Main Methods:
- Quantitative reverse transcription PCR (qRT-PCR) for gene expression analysis.
- Cell proliferation (EdU) and apoptosis assays.
- Dual luciferase reporter assays, qRT-PCR, and Western blotting to confirm molecular interactions.
Main Results:
- CMR expression was upregulated in S. aureus-infected BMECs, promoting inflammatory factors.
- Silencing CMR inhibited cell proliferation and induced apoptosis in mammary epithelial cells.
- CMR functions as a competing endogenous RNA (ceRNA) for miR-877, upregulating FOXM1 expression.
Conclusions:
- CMR regulates autoprotection against S. aureus mastitis in BMECs via the miR-877/FOXM1 axis.
- This pathway influences immune responses in dairy cow mammary tissues and cells.
- Findings provide a basis for developing targeted therapies for cow mastitis.
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