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牛乳腺上皮细胞中受 和 损伤的 N6-甲基腺苷修饰的 circRNA

N-Methyladenosine-Modified circRNA in the Bovine Mammary Epithelial Cells Injured by and .

机构信息

Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, China.

State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural University, Wuhan, China.

出版信息

Front Immunol. 2022 Apr 4;13:873330. doi: 10.3389/fimmu.2022.873330. eCollection 2022.

DOI:10.3389/fimmu.2022.873330
PMID:35444650
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9014013/
Abstract

Mastitis is a common disease that hinders the development of dairy industry and animal husbandry. It leads to the abuse of antibiotics and the emergence of super drug-resistant bacteria, and poses a great threat to human food health and safety. () and () are the most common pathogens of mastitis in dairy cows and usually cause subclinical or clinical mastitis. CircRNAs and N-methyladenosine (mA) play important roles in immunological diseases. However, the mechanisms by which mA modifies circRNA in bovine mammary epithelial cells remain poorly understood. The aim of our study was to investigate mA-modified circRNAs in bovine mammary epithelial cells (MAC-T cells) injured by and The profile of mA-modified circRNA showed a total of 1,599 mA peaks within 1,035 circRNAs in the control group, 35 peaks within 32 circRNAs in the group, and 1,016 peaks within 728 circRNAs in the group. Compared with the control group, 67 peaks within 63 circRNAs were significantly different in the group, and 192 peaks within 137 circRNAs were significantly different in the group. Furthermore, we found the source genes of these differentially mA-modified circRNAs in the and groups with similar functions according to GO and KEGG analyses, which were mainly associated with cell injury, such as inflammation, apoptosis, and autophagy. CircRNA-miRNA-mRNA interaction networks predicted the potential circRNA regulation mechanism in and -induced cell injury. We found that the mRNAs in the networks, such as BCL2, MIF, and TNFAIP8L2, greatly participated in the MAPK, WNT, and inflammation pathways. This is the first report on mA-modified circRNA regulation of cells under and treatment, and sheds new light on potential mechanisms and targets from the perspective of epigenetic modification in mastitis and other inflammatory diseases.

摘要

乳腺炎是一种常见的疾病,它阻碍了奶牛养殖业的发展。它导致了抗生素的滥用和超级耐药菌的出现,对人类的食品安全构成了巨大威胁。()和()是奶牛乳腺炎最常见的病原体,通常引起亚临床或临床乳腺炎。环状 RNA 和 N6-甲基腺苷(mA)在免疫性疾病中发挥重要作用。然而,mA 修饰牛乳腺上皮细胞中环状 RNA 的机制仍知之甚少。本研究旨在探讨()和()损伤的牛乳腺上皮细胞(MAC-T 细胞)中的 mA 修饰环状 RNA。mA 修饰环状 RNA 的图谱显示,对照组中共有 1035 个环状 RNA 中有 1599 个 mA 峰,组中有 32 个环状 RNA 中有 35 个峰,组中有 728 个环状 RNA 中有 1016 个峰。与对照组相比,组中 67 个环状 RNA 中有 63 个 mA 峰差异显著,组中 192 个环状 RNA 中有 137 个 mA 峰差异显著。此外,根据 GO 和 KEGG 分析,我们发现这些差异 mA 修饰环状 RNA 在()和()组中的同源基因具有相似的功能,主要与细胞损伤有关,如炎症、凋亡和自噬。环状 RNA-miRNA-mRNA 相互作用网络预测了()和()诱导细胞损伤中潜在的环状 RNA 调控机制。我们发现,网络中的 mRNAs,如 BCL2、MIF 和 TNFAIP8L2,极大地参与了 MAPK、WNT 和炎症途径。这是首次报道 mA 修饰环状 RNA 对()和()处理细胞的调控,从表观遗传修饰的角度为乳腺炎和其他炎症性疾病的潜在机制和靶点提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/2d97c4f571a3/fimmu-13-873330-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/aff374e20c6a/fimmu-13-873330-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/495b183e185f/fimmu-13-873330-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/7ee971e97434/fimmu-13-873330-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/b58a93595d49/fimmu-13-873330-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/6b774c303bc4/fimmu-13-873330-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/e6ebdd618e51/fimmu-13-873330-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/9ac3453e3a2d/fimmu-13-873330-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/2d97c4f571a3/fimmu-13-873330-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/aff374e20c6a/fimmu-13-873330-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/495b183e185f/fimmu-13-873330-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/7ee971e97434/fimmu-13-873330-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/b58a93595d49/fimmu-13-873330-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/6b774c303bc4/fimmu-13-873330-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/e6ebdd618e51/fimmu-13-873330-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/9ac3453e3a2d/fimmu-13-873330-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f3b0/9014013/2d97c4f571a3/fimmu-13-873330-g008.jpg

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