相关实验视频

Updated: Jul 9, 2025

Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery

Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery

Published on: February 14, 2017

抑制PFKFB3的表达刺激了巨介导的淋巴细胞发生在急性心肌梗塞后

Tianyi Cui¹, Chao Feng^2,3, Hantao Jiang²

¹State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, 301617 Tianjin, China.

Frontiers in bioscience (Landmark edition)

|December 8, 2023

概括

抑制巨细胞中的PFKFB3可能会促进VEGF-C的产生,促进淋巴血管生成,减少心脏损伤后的炎症. 这一发现为治疗心力衰竭和心肌梗塞提供了新的见解.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
血管生物学血管生物学

背景情况:

淋巴血管扩张对心脏功能至关重要;功能受损可能导致心力衰竭 (HF) 和急性心肌梗塞 (AMI).
巨细胞通过血管内皮细胞生长因子C (VEGF-C) 促进淋巴血管生成,但确切的机制需要澄清.

研究的目的:

研究巨细胞糖解酶 PFKFB3 在调节 VEGF-C 生产和淋巴血管生成中的作用.
探索向巨细胞PFKFB3的治疗潜力,以减轻心脏损伤.

主要方法:

腺相关病毒 (AAV9) 在心脏组织中介于体内VEGFR3基因调节.
使用转基因小鼠 (Lyz2Cre,VEGFCfl/fl,PFKFB3fl/fl) 来评估巨细胞特异性基因淘汰效应.
采用流细胞计,光染色,qPCR和海马实验来分析心脏功能,淋巴结碎片,基因表达和巨细胞糖解.

主要成果:

心脏组织中VEGFR3的升级改善了心脏功能,并减少了再生输液损伤后的纤维化.
骨髓细胞VEGF-C缺乏症在再注射后加剧了炎症和巨细胞的积累.
抑制巨糖解酶PFKFB3刺激了VEGF-C的产生,并诱导了淋巴血管生成,改善了转流损伤后的结果.

结论:

抑制巨细胞PFKFB3可以增强VEGF-C的表达,从而促进淋巴血管生成.
向巨细胞PFKFB3可能代表了一种新的治疗策略,以减轻炎症效应并改善缺血-再输液 (I/R) 损伤后的心脏功能.

关键词:

缺血-再输血损伤的损伤淋巴血管生成 (Lymphangiogenesis) 是一种导致淋巴血管发生的过程.巨细胞是什么?巨细胞是什么?

更多相关视频

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation

Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation

Published on: April 3, 2017

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

相关概念视频

Regulation of Angiogenesis and Blood Supply

Regulation of Angiogenesis and Blood Supply

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...