SMYD2通过与肌肉激素的相互作用来调节血管光滑肌细胞表型切换和内脏增生
Yu Zhou1,2, Shaligram Sharma3, Xiaonan Sun3
1Center for Molecular and Translational Medicine, Institute for Biomedical Sciences, Georgia State University, 157 Decatur St SE, Atlanta, GA, 30303, USA. zhouy259@mail3.sysu.edu.cn.
Cellular and molecular life sciences : CMLS
|August 24, 2023
概括
含有SET和MYND域的蛋白2 (SMYD2) 调节血管光滑肌细胞 (VSMC) 的功能. 失去了SMYD2会恶化内增生症,而它的增加会通过涉及肌肉细胞的表观遗传机制来抑制VSMC的增殖和迁移.
科学领域:
- 血管生物学 血管生物学
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 细胞平衡是细胞的平衡.
背景情况:
- 含有SET和MYND域的蛋白2 (SMYD2) 与致癌和炎症有关.
- 它在血管光滑肌细胞 (VSMC) 稳态和血管疾病中的作用尚不清楚.
研究的目的:
- 调查SMYD2在VSMC表型调制和血管内皮增生症中的功能.
- 阐明SMYD2在这些过程中的作用背后的分子机制.
主要方法:
- 使用了一个特定于SMC的SMYD2淘汰赛小鼠模型.
- 进行了体外研究,包括VSMC扩散和迁移试验.
- 进行了全基因组转录组分析和功能丧失/增益研究.
主要成果:
- 在受伤的动脉和表型调节的VSMC中,SMYD2的表达减少.
- SMYD2 缺陷加剧了新密的形成,而过度表达抑制了VSMC的增殖和迁移.
- SMYD2通过肌肉激素依赖的表观遗传调节,提高了收缩基因表达的调节,并通过肌肉激素依赖的表观遗传调节抑制了VSMC的增殖/迁移.
结论:
- SMYD2是VSMC收缩表型和内增生症的新型调节剂.
- SMYD2通过肌肉内依赖的表观遗传机制起作用,影响SMC收缩基因促进者的染色质状态.
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