在皮层神经元中,BMECs通过VEGF介导的葡萄糖摄入调节来改善高葡萄糖诱导的形态异常和突触功能障碍
Yu-Qi Huang1,2, Xiao Gu1,2, Xiao Chen1,2
1Department of Neurobiology and Research Institute for Aging and Medicine, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, 138 Yi-Xue-Yuan Road, Shanghai, 200032, People's Republic of China.
Cellular and molecular neurobiology
|July 7, 2023
概括
大脑的微血管内皮细胞通过释放血管内皮生长因子 (VEGF) 来保护糖尿病中高葡萄糖诱导的神经元退化. 这一发现为糖尿病痴呆症提供了新的治疗策略.
科学领域:
- 神经科学是一个神经科学.
- 内分泌学 在内分泌学.
- 细胞生物学 细胞生物学
背景情况:
- 糖尿病与大脑神经元退化和认知能力下降有关.
- 神经血管相互作用对大脑功能至关重要,但内皮细胞在糖尿病神经退行症中的作用尚不清楚.
研究的目的:
- 为了研究大脑微血管内皮细胞 (BMEC) 对高葡萄糖诱导的神经性损的作用.
- 探索涉及血管内皮生长因子 (VEGF) 的潜在机制.
主要方法:
- 在高葡萄糖条件下与神经元一起培养BMEC.
- 免疫光标记和西部斑点用于神经元外生和突触.
- 活细胞成像用于神经元葡萄糖转运器吸收.
- 用BMEC条件介质 (B-CM) 和VEGF的治疗.
主要成果:
- BMECs显著降低了高葡萄糖诱导的神经元外生和突触生成的抑制.
- BMECs保留了神经元的葡萄糖吸收能力,这种效应被B-CM和VEGF模仿.
- 用SU1498阻断VEGF受体消除了BMEC和B-CM的保护作用.
结论:
- 大脑微血管内皮细胞通过VEGF释放和受体激活来保护神经元免受高血糖引起的损伤.
- 这突显了神经血管合在糖尿病大脑病理学中的关键作用.
- 这些发现表明,预防或治疗糖尿病痴呆症的新治疗途径.
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