Faculty of Food Science and Engineering, Kunming University of Science and Technology, Kunming 650500, China.
Key Laboratory of Dairy Science of Education Ministry, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Int J Mol Sci. 2023 Sep 20;24(18):14352. doi: 10.3390/ijms241814352.
The mammary gland undergoes intensive remodeling during the lactation cycle, and the involution process of mammary gland contains extensive epithelial cells involved in the process of autophagy. Our studies of mice mammary glands suggest that miR-30a-3p expression was low during involution compared with its high expression in the mammary glands of lactating mice. Then, we revealed that miR-30a-3p negatively regulated autophagy by autophagy related 12 () in mouse mammary gland epithelial cells (MMECs). Restoring ATG12, knocking down autophagy related 5 (), starvation, and Rapamycin were used to further confirm this conclusion. Overexpression of miR-30a-3p inhibited autophagy and altered mammary structure in the involution of the mammary glands of mice, which was indicative of alteration in mammary remodeling. Taken together, these results elucidated the molecular mechanisms of miR-30a-3p as a key induction mediator of autophagy by targeting within the transition period between lactation and involution in mammary glands.
乳腺在哺乳期经历强烈的重塑，乳腺的退化过程包含广泛涉及自噬过程的上皮细胞。我们对小鼠乳腺的研究表明，与哺乳期小鼠乳腺中的高表达相比，乳腺退化过程中 miR-30a-3p 的表达较低。然后，我们揭示了 miR-30a-3p 通过自噬相关蛋白 12（）负调控小鼠乳腺上皮细胞（MMECs）中的自噬。恢复 ATG12、敲低自噬相关蛋白 5（）、饥饿和雷帕霉素进一步证实了这一结论。miR-30a-3p 的过表达抑制自噬并改变了小鼠乳腺的退化结构，表明乳腺重塑发生改变。综上所述，这些结果阐明了 miR-30a-3p 通过靶向在哺乳期和乳腺退化过渡期之间作为自噬的关键诱导介质的分子机制。
