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在水静压下,米勒细胞通过TRPV1/PLCγ1复合体介导的流来调节视网膜细胞存活率,在实验性玻璃眼中

Huiling Hu¹, Danyao Nie¹, Min Fang²

¹Department of Cataract, Shenzhen Eye Hospital, Shenzhen Eye Institute, Jinan University, Shenzhen, China.

The FEBS journal

|February 23, 2024

概括

在青光眼中,眼压升高会通过TRPV1和PLCγ1.1增加Müller细胞中的ATP和. 抑制这些通路和P2X7可以减少视网膜质细胞死亡.

科学领域:

眼科医生眼科眼科
神经科学是一个神经科学.
细胞生物学细胞生物学

背景情况:

玻璃眼是一种不可逆转的致盲疾病,病理机制不明确.
眼内压升高 (IOP) 是青光眼的主要风险因素.
穆勒细胞和视网膜质细胞 (RGCs) 在视网膜功能和疾病发病过程中至关重要.

研究的目的:

为了研究TRPV1,PLCγ1和P2X7在调节细胞内 (Ca2+) 和腺三酸盐 (ATP) 在高IOP下的Müller细胞和RGC中的作用.
探索抑制这些途径的治疗潜力,以抑制RGC在青光眼中的存活.

主要方法:

在水静压下 (HP) 使用的米勒细胞和用条件介质培养的RGC.
采用siRNA来抑制TRPV1,PLCγ1和P2X7在各自细胞类型中的表达.
建立了慢性眼高血压 (COH) 的小鼠模型,用于体内验证.

主要成果:

惠普增加了Müller细胞中的ATP和Ca2+流入,上调TRPV1和p-PLCγ1.
在米勒细胞中抑制TRPV1或PLCγ1减少了HP诱导的ATP和Ca2+积累.
击败TRPV1,PLCγ1或P2X7降低了RGC亡和自 in vitro和 in vivo.

结论:

TRPV1和PLCγ1调解HP诱导的穆勒细胞变化,影响RGC存活率.
在这些条件下,RGC中的P2X7也会导致亡和自.
抑制TRPV1/PLCγ1和P2X7通路为绿眼提供了潜在的治疗策略.

关键词:

穆勒细胞是什么意思?这是一个P2X7的P2X7.在 PLCγ1γ1 中.在RGC中,RGC是指RGC.在 TRPV1 中.水静压的压力是水静压.

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