长非编码RNA (CMR) 通过调节miR-877/FOXM1参与乳牛S. aureus乳腺炎的自我保护
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.
Ecotoxicology and environmental safety
|May 14, 2024
概括
长非编码RNA (LncRNA) CMR通过调节miR-877/FOXM1通路,在奶牛中促进金黄色乳腺炎. 抑制CMR可以提高奶牛乳细胞免疫力,减少炎症,为乳腺炎提供新的治疗点.
科学领域:
- 兽医免疫学 兽医免疫学
- 分子生物学分子生物学
- 乳制品科学 乳制品科学
背景情况:
- 长非编码RNAs (LncRNAs) 与人类疾病有关,但它们在牛乳腺炎中的作用未得到充分研究.
- 由S. aureus引起的牛乳炎对乳制品生产和动物福利产生重大影响.
研究的目的:
- 为了研究S. aureus乳腺炎期间在牛乳腺上皮细胞 (BMEC) 中特定的LncRNA (CMR) 的机制.
- 阐明牛乳腺炎自保护中涉及LncRNAs,microRNAs和mRNAs的调节途径.
主要方法:
- 定量逆转录PCR (qRT-PCR) 用于基因表达分析.
- 细胞增殖 (EdU) 和细胞亡测定.
- 双 luciferase 记者测定,qRT-PCR 和 Western 涂抹以确认分子相互作用.
主要成果:
- 在被S. aureus感染的BMEC中,CMR表达上调,促进炎症因素.
- 沉默CMR抑制了细胞增殖,并在乳腺上皮细胞中诱导了细胞亡.
- 对于miR-877来说,CMR作为竞争的内源RNA (ceRNA) 起作用,对FOXM1的表达进行上调.
结论:
- 在BMEC中,CMR通过miR-877/FOXM1轴调节对S. aureus乳腺炎的自我保护.
- 这一途径影响乳牛乳腺组织和细胞中的免疫反应.
- 这些发现为开发针对牛乳腺炎的向治疗提供了基础.
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