相关实验视频
Updated: Jun 25, 2025

08:02
Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice
Published on: October 19, 2013
18.3K
SMYD2-甲基化PPARγ通过激活线粒细胞衰变促进缺氧诱导的肺高血压
Yi Li1, Xiang Wei1,2,3,4, Rui Xiao5,6
1Division of Cardiovascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China (Y.L., X. Wei, T.X., Z.-M.F., B.H., X.G., H.L., X.-H.Z., D.-S.J.).
Circulation research
|May 21, 2024
概括
抑制变异性,增强性,三胸和骨髓神经DEAF-1域含蛋白2 (SMYD2) 的抑制剂通过抑制PPARγ驱动肺高血压 (PH). 准SMYD2或激活PPARγ可能会阻止PH.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 细胞病理生理学
背景情况:
- 肺高血压 (PH) 的特点是肺动脉光滑肌肉细胞 (PASMC) 的高增殖和血管重塑.
- 蛋白质甲基化在PASMC增殖和PH中的作用涉及,但机制尚不清楚.
研究的目的:
- 调查氨基甲基转移酶SMYD2在PH病变发生中的作用.
- 阐明SMYD2影响PASMC增殖和PH发育的分子机制.
主要方法:
- 使用慢性缺氧诱导的PH大鼠和小鼠模型,SMYD2-转基因小鼠,以及用LLY-507.7抑制SMYD2的SMYD2抑制.
- 采用初级培养大鼠PASMCs与SMYD2敲击或过度表达,以研究繁殖和机制.
- 研究了SMYD2与PPARγ的相互作用及其对核转位和转录活性的影响.
主要成果:
- 在PH和缺氧暴露的PASMC中,SMYD2表达被上调.
- 抑制SMYD2减弱了PH的发展和PASMC的过度扩散;SMYD2的过度表达加剧了PH.
- SMYD2单甲基化PPARγ,抑制其核转位和活性,促进线粒和PASMC扩散.
结论:
- SMYD2通过抑制PPARγ和促进线粒细胞衰变来加速PASMC的增殖和PH.
- 准SMYD2或激活PPARγ为PH预防提供了潜在的治疗策略.
相关概念视频
Regulation of Angiogenesis and Blood Supply
2.6K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
2.6K
Abnormal Proliferation
4.5K
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
Adaptive Mechanisms in Cancer Cells
5.7K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.7K
PI3K/mTOR/AKT Signaling Pathway
3.5K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.5K

