γ干扰素通过c-Abl/HDAC2信号通路调节乳腺上皮细胞恶性生长（英文）

目的:在之前的研究中我们发现γ干扰素(IFN-γ)通过营养感受器GCN2诱导牛乳腺上皮细胞(BMEC)的恶性转化。在恶性转化的表型中,包括细胞周期缩短、细胞增殖增加、细胞迁移和侵袭的发生,而细胞生长的异常调节是细胞恶性转化的第一步。因此,本研究旨在探讨IFN-γ诱导细胞恶性生长的分子机制。创新点:实验对象γ-BMEC能够更好的用于乳腺癌发生的基础研究,是一种新的研究工具。我们选择恶性细胞生长来详细研究IFN-γ的作用机制,为IFN-γ、恶性细胞生长甚至乳腺癌之间的密切关系提供直接证据。方法:通过MTT实验检测IFN-γ长期刺激下细胞的增殖能力;蛋白质印迹(Westernblot)检测cyclin D1/CDK4、p21、HDAC2、c-Abl蛋白的表达;免疫荧光观察c-Abl入核。结论:IFN-γ通过c-Abl/HDAC2信号通路促进恶性BMEC的生长。     

Integrated metabolism and epigenetic modifications in the macrophages of mice in responses to cold stress

The negative effects of low temperature can readily induce a variety of diseases. We sought to understand the reasons why cold stress induces disease by studying the mechanisms of fine-tuning in macrophages following cold exposure. We found that cold stress triggers increased macrophage activation accompanied by metabolic reprogramming of aerobic glycolysis. The discovery, by genome-wide RNA sequencing, of defective mitochondria in mice macrophages following cold exposure indicated that mitochondrial defects may contribute to this process. In addition, changes in metabolism drive the differentiation of macrophages by affecting histone modifications. Finally, we showed that histone acetylation and lactylation are modulators of macrophage differentiation following cold exposure. Collectively, metabolism-related epigenetic modifications are essential for the differentiation of macrophages in cold-stressed mice, and the regulation of metabolism may be crucial for alleviating the harm induced by cold stress.     

Epigenetic regulation of adipocyte differentiation and adipogenesis

It is generally agreed that adipocytes originate from mesenchymal stem cells in what can be divided into two processes: determination and differentiation. In the past decade, many factors associated with epigenetic signals have been proved to be pivotal for the appropriate timing of adipogenesis progression. A large number of coregulators at critical gene promoters set up specific patterns of DNA methylation, histone acetylation and methylation, and nucleosome rearrangement, that act as an epigenetic code to modulate the correct progress of adipocyte differentiation and adipogenesis during adipogenesis. In this review, we focus on the functions and roles of epigenetic processes in preadipocyte differentiation and adipogenesis.