相关实验视频
Updated: Jun 30, 2025

07:35
Gene Transfer for Ischemic Heart Failure in a Preclinical Model
Published on: May 15, 2011
12.9K
患有心脏病和心脏衰竭的细胞外小囊加速瘤的生长
Tal Caller1,2, Itai Rotem1,2, Olga Shaihov-Teper1,2
1Neufeld and Tamman Cardiovascular Research Institutes, School of Medicine, Tel Aviv University, Israel (T.C., I.R., O.S.-T., D.L., Y.S., R.S., M.N., N.N.-S., J.L.).
Circulation
|March 15, 2024
概括
心肌梗塞 (MI) 后心脏中的小细胞外囊 (sEV) 促进癌症生长. 使用螺旋减少了这种效应,为心脏功能障碍和癌症之间的联系提供了潜在的治疗策略.
科学领域:
- 心脏病学
- 癌症学
- 细胞外膀生物学
背景情况:
- 心肌梗塞 (MI) 和心力衰竭与癌症发生率的增加有关.
- 连接心脏功能障碍和癌症的根本机制尚不清楚.
- 心脏小细胞外囊 (sEVs) 被研究为潜在的调解器.
研究的目的:
- 测试心脏介质层细胞衍生的sEVs (cMSC-sEVs) 与心脏病发作后的左室功能障碍 (LVD) 与癌症的联系的假设.
- 分析cMSC-sEVs对癌细胞和瘤生长的影响.
- 评估螺旋作为一个治疗干预.
主要方法:
- 从MI后的心脏和培养的cMSC中净化和表征sEV.
- 对cMSC-EV货物的蛋白质组分析.
- 在体外评估cMSC-sEV对癌细胞,巨细胞和内皮细胞的影响.
- 在MI后LVD小鼠的体内瘤建模,包括sEV转移和耗尽研究.
- 对螺旋治疗的评估.
主要成果:
- 与没有失败的心脏相比,心脏和cMSC产生的sEV具有促进瘤的负载.
- 在体外和体内的肺癌和结肠癌增长加速.
- 在患有LVD的小鼠中,继发性转移后的cMSC- sEV增加了瘤大小和扩散.
- 降低了与心脏病相关的瘤增长,而螺旋乳治疗抑制了瘤的生长.
结论:
- 来自心脏病发作后的心脏病发作,特别是cMSC-sEV,含有前原因子.
- 癌细胞吸收这些SEV会增加瘤的生长.
- 螺旋乳治疗有效地减少了心脏病发作后瘤的加速生长,这表明了治疗途径.
相关概念视频
The Tumor Microenvironment
6.6K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
6.6K
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
Metastasis
5.5K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.5K
Cancer Cell Migration through Invadopodia
2.3K
Invadosome is a broad category of cell surface structures with proteolytic activity that degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
2.3K

