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首页> 外文期刊>Cell biology international. >Low-dose rotenone exposure induces early senescence leading to late apoptotic signaling cascade in human trabecular meshwork (HTM) cell line: An in vitro glaucoma model
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Low-dose rotenone exposure induces early senescence leading to late apoptotic signaling cascade in human trabecular meshwork (HTM) cell line: An in vitro glaucoma model

机译：低剂量鱼藤酮暴露诱导人小梁网（HTM）细胞系早期衰老，导致晚期凋亡信号传导级联：体外青光眼模型

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This study aimed to determine whether the prolonged exposure of the human trabecular meshwork (HTM) cell line to a low dose (1 nM) of rotenone could simulate a glaucomatous-like condition and serve as a cellular model for its etiological analysis. Under 1-nM rotenone exposure for 24-72 h, HTM cells showed a decrease in cell viability as assessed by an MTT assay and showed mitochondrial dysfunction as assessed by measuring H(2)DCFDA fluorescence; a decrease in ATP level was also observed. Flow cytometric analysis showed an increase in cellular size and granularity. Elevated AF showed initial senescence. LF staining with SBB and its spectrofluorometric quantification confirmed growth arrest. An accumulation of cytoplasmic myocilin, IL-6, and MMP-9 at 72 h of exposure supported glaucomatous induction. TEM revealed morphological changes in mitochondria and nuclei of treated cells. Signaling cascades were assessed by immunoblotting and immunocytochemical analysis. This study showed a shift in status of the cells from initial senescence to induction of apoptosis in the HTM cell line due to continuous low-dose exposure to rotenone; however, at 72 h, both senescence and apoptotic features are apparent in these cells. This is the first report that reveals the potential of a prolonged low-dose exposure of rotenone to simulate senescence in the HTM cell line to cause a glaucomatous condition.
机译：这项研究旨在确定人类小梁网（HTM）细胞系长时间暴露于低剂量（1 nM）鱼藤酮是否可以模拟青光眼样疾病并作为其病因分析的细胞模型。在1-nM鱼藤酮暴露下24-72小时，通过MTT分析评估，HTM细胞显示出细胞活力降低，而通过测量H（2）DCFDA荧光评估，则显示出线粒体功能障碍。还观察到ATP水平降低。流式细胞仪分析显示细胞大小和粒度增加。升高的AF显示初始衰老。用SBB进行LF染色及其荧光分光光度法证实了生长停滞。暴露72 h时细胞质肌球蛋白，IL-6和MMP-9的积累支持青光眼的诱导。 TEM显示了处理过的细胞的线粒体和细胞核的形态变化。通过免疫印迹和免疫细胞化学分析评估信号传导级联。这项研究表明，由于连续不断的低剂量鱼藤酮暴露，HTM细胞系的细胞状态从最初的衰老转变为诱导细胞凋亡。然而，在72小时时，这些细胞的衰老和凋亡特征均明显。这是第一份报告，揭示了长期低剂量鱼藤酮暴露可能模拟HTM细胞系中的衰老，从而导致青光眼。

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