Ma Xinhao, Zhang Dianqi, Yang Zhimei, Sun Meijun, Mei Chugang, Zan Linsen
College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, PR China.
College of Grassland Agriculture, Northwest A&F University, Yangling, Shaanxi 712100, PR China; National Beef Cattle Improvement Center, Northwest A&F University, Yangling, Shaanxi 712100, PR China.
Int J Biol Macromol. 2025 Jan;286:138082. doi: 10.1016/j.ijbiomac.2024.138082. Epub 2024 Nov 26.
Intramuscular fat (IMF) plays a crucial role in enhancing the tenderness, flavor, and juiciness of beef, making the increase of IMF content a significant objective in beef breeding. A key factor influencing IMF levels is the number of intramuscular preadipocytes. Previous studies have indicated a correlation between bta-miR-484 and IMF content. In this study, we found that bta-miR-484 is differentially expressed during the proliferation of intramuscular preadipocytes. Our research identified that bta-miR-484 targets MAP3K9, revealing a novel mechanism for regulating both proliferation and apoptosis via the JNK signaling pathway. Functional gain and loss experiments demonstrated that bta-miR-484 inhibits the transition of bovine intramuscular preadipocytes from the G0/G1 phase to the S phase, and significant increase the proportion of early apoptotic cells. Additionally, miRNA pulldown and luciferase reporter assays confirmed MAP3K9 as the target gene of bta-miR-484. Furthermore, rescue experiments indicated that bta-miR-484 mediates its effects on proliferation and apoptosis through the MAP3K9/JNK/CCND1 and MAP3K9/JNK/BCL2 axes. These findings suggest that bta-miR-484 is a non-coding RNA that inhibits the proliferation and promotes the apoptosis of intramuscular preadipocytes, indicating that treatment with bta-miR-484 may offers a novel strategy for enhancing IMF content.
肌内脂肪(IMF)在提高牛肉的嫩度、风味和多汁性方面起着至关重要的作用,因此提高IMF含量成为肉牛育种的一个重要目标。影响IMF水平的一个关键因素是肌内前脂肪细胞的数量。先前的研究表明bta-miR-484与IMF含量之间存在相关性。在本研究中,我们发现bta-miR-484在肌内前脂肪细胞增殖过程中存在差异表达。我们的研究确定bta-miR-484靶向MAP3K9,揭示了一种通过JNK信号通路调节增殖和凋亡的新机制。功能获得和缺失实验表明,bta-miR-484抑制牛肌内前脂肪细胞从G0/G1期向S期的转变,并显著增加早期凋亡细胞的比例。此外,miRNA下拉和荧光素酶报告基因检测证实MAP3K9是bta-miR-484的靶基因。此外,拯救实验表明,bta-miR-484通过MAP3K9/JNK/CCND1和MAP3K9/JNK/BCL2轴介导其对增殖和凋亡的影响。这些发现表明,bta-miR-484是一种抑制肌内前脂肪细胞增殖并促进其凋亡的非编码RNA,这表明用bta-miR-484处理可能为提高IMF含量提供一种新策略。