Jiayi Zhou
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Jiayi Zhou has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Feng-Qi Zhao
Department of Animal and Veterinary Sciences, University of Vermont, Burlington, VT 05405
1 shared publication - Shuangfeng Chu
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
1 shared publication - Tianqi Zhao
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
1 shared publication - Xubin Lu
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
1 shared publication - Yadan Chen
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
1 shared publication - Yujia Sun
College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
1 shared publication
Latest Publications
- Open Access
LncRNA BMNCR Regulates Proliferation, Apoptosis and Inflammatory Response in Bovine Mammary Epithelial Cells Through the miR-145/ANO6 Axis
Bovine mastitis causes significant economic losses in the dairy industry. Emerging evidence highlights the critical role of long non-coding RNAs (lncRNAs) in inflammation-associated epigenetic regulation through competing endogenous RNA (ceRNA) networks. In this study, we established a bovine mastitis model in three healthy primiparous Holstein cows by intramammary infection with S. aureus. Infected and control mammary tissue samples were then collected for transcriptomic profiling, which identified 2005 differentially expressed lncRNAs. Among them, BMNCR was significantly upregulated in S. aureus-infected mammary tissues and S. aureus-stimulated BMECs. We evaluated the coding potential of BMNCR and confirmed its non-coding nature. Functional studies in BMECs demonstrated that knockdown of BMNCR suppressed proliferation, promoted apoptosis, and altered the expression of inflammatory factors, including IL-2, IL-6, IL-8, and IL-12. Mechanistically, BMNCR acted as a sponge for bta-miR-145, thereby leading to the derepression of ANO6. Silencing ANO6 partly recapitulated the effects of BMNCR knockdown, impairing proliferation and increasing IL-8 expression. Collectively, these findings suggest that the BMNCR/miR-145/ANO6 axis is involved in the regulation of inflammatory responses and epithelial homeostasis during bovine mastitis, with BMNCR functioning as a protective regulator in this process.
Open AccessLncRNA BMNCR Regulates Proliferation, Apoptosis and Inflammatory Response in Bovine Mammary Epithelial Cells Through the miR-145/ANO6 Axis
Bovine mastitis causes significant economic losses in the dairy industry. Emerging evidence highlights the critical role of long non-coding RNAs (lncRNAs) in inflammation-associated epigenetic regulation through competing endogenous RNA (ceRNA) networks. In this study, we established a bovine mastitis model in three healthy primiparous Holstein cows by intramammary infection with S. aureus. Infected and control mammary tissue samples were then collected for transcriptomic profiling, which identified 2005 differentially expressed lncRNAs. Among them, BMNCR was significantly upregulated in S. aureus-infected mammary tissues and S. aureus-stimulated BMECs. We evaluated the coding potential of BMNCR and confirmed its non-coding nature. Functional studies in BMECs demonstrated that knockdown of BMNCR suppressed proliferation, promoted apoptosis, and altered the expression of inflammatory factors, including IL-2, IL-6, IL-8, and IL-12. Mechanistically, BMNCR acted as a sponge for bta-miR-145, thereby leading to the derepression of ANO6. Silencing ANO6 partly recapitulated the effects of BMNCR knockdown, impairing proliferation and increasing IL-8 expression. Collectively, these findings suggest that the BMNCR/miR-145/ANO6 axis is involved in the regulation of inflammatory responses and epithelial homeostasis during bovine mastitis, with BMNCR functioning as a protective regulator in this process.