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缺氧压力通过HIF-1α/GDNF/LOXL2轴促进了星球细胞透式的生长

Zimu Li¹, Shun Xi², Ziqi Zhang²

¹Department of Neurobiology and Cell Biology, Xuzhou Key Laboratory of Neurobiology, National Demonstration Center for Experimental Basic Medical Science Education, Xuzhou Medical University, Xuzhou 221004, Jiangsu, China; Clinical Medicine Research Center, The Suqian Clinical College of Xuzhou Medical University, Suqian 223800, Jiangsu, China.

Biochimica et biophysica acta. Molecular basis of disease

|February 2, 2025

概括

缺氧会增加星球细胞中的质细胞系衍生神经营养因子 (GDNF),通过HIF-1α/GDNF/P-CREB通路促进星球瘤的生长. 抑制这种途径会减少星球细胞的激活和透生长.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
在瘤学瘤学.

背景情况:

质细胞系衍生神经营养因子 (GDNF) 与星瘤的发展有关.
在缺氧下驱动GDNF介导的星细胞转变的确切机制尚不清楚.

研究的目的:

阐明缺氧诱导天体细胞激活并促进天体瘤进展的分子机制.
调查缺氧诱导因子1-alpha (HIF-1α) 和GDNF信号轴在天体细胞介导的瘤发生中的作用.

主要方法:

主要的老鼠和人类星体细胞,以及C6质瘤细胞,都经历了缺氧条件.
测量了GDNF,HIF-1α和酸氧化酶样蛋白2 (LOXL2) 的表达水平.
使用Luciferase记者测试来评估促进体结合.
分析了涉及ERK,P38和CREB酸化的信号通路.
功能性测试评估了细胞活力,迁移和上皮层-介质细胞过渡 (EMT).

主要成果:

缺氧显著上调了星球细胞中的GDNF表达,与HIF-1α激活相关,并增加了与GDNF促进剂的结合.
当高GDNF进一步激活HIF-1α时,观察到一个积极的反循环.
低氧诱导的LOXL2表达,GDNF的下游目标,通过HIF-1α/GDNF/P-CREB信号轴.
抑制GDNF信号传递或LOXL2抑制的缺氧诱导的天体细胞激活,迁移和EMT.

结论:

缺氧会通过HIF-1α/GDNF/P-CREB通路触发星球细胞激活和LOXL2上调.
这种信号级联促进了星球细胞的透和星球瘤细胞的攻击性生长.
准HIF-1α/GDNF/LOXL2轴为星瘤提供了一个潜在的治疗策略.

关键词:

星球细胞是星球细胞.星光瘤是一个天文瘤.这就是GDNF的原因.氧气过低是因为缺氧.在LOXL2中使用LOXL2.

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