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首页> 外文期刊>Journal of cellular physiology. >TIGAR impedes compression-induced intervertebral disc degeneration by suppressing nucleus pulposus cell apoptosis and autophagy
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TIGAR impedes compression-induced intervertebral disc degeneration by suppressing nucleus pulposus cell apoptosis and autophagy

机译：TIGAR阻碍compression-induced椎间椎间盘变性,抑制髓核细胞凋亡和自噬

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摘要

To investigate whether TP53-induced glycolysis and apoptosis regulator (TIGAR) participates in compression-induced intervertebral disc (IVD) degeneration, and to determine the regulatory effect of TIGAR on nucleus pulposus (NP) cell autophagy and apoptosis following compression-induced injuries. IVD tissues were collected from human patients undergoing surgery (n = 20) and skeletally mature Sprague-Dawley rats (n = 15). Initially, the effect of compression on the expression of TIGAR was evaluated with in vivo and in vitro models. In addition, TIGAR was silenced to investigate the regulatory effect of TIGAR on compression-induced intracellular reactive oxygen species (ROS) levels, autophagy, and apoptosis in rat NP cells. Furthermore, the P53 inhibitor pifithrin-α (PFTα) and SP1 inhibitor mithramycin A were employed to detect expression level changes of TIGAR and autophagy-associated target molecules. TIGAR expression of NP cells increased gradually in human degenerative IVDs and in rat NP cells under compression both in vivo and in vitro. TIGAR knockdown enhanced compression-induced intracellular ROS generation and the NADPH/NADP+ and GSH/GSSG ratios. Moreover, TIGAR knockdown amplified the compression-induced caspase-3 activation and the apoptosis rate of rat NP cells. Likewise, knockdown of TIGAR significantly accelerated LC3B expression and autophagosome formation in rat NP cells during compression-induced injuries. The results also established that mithramycin A could inhibit TIGAR expression and autophagy levels in NP cells under compression conditions, while PFTa had no similar effect. Our data demonstrated that TIGAR acted as an important endogenous negative regulator of ROS levels, which might inhibit compression-induced apoptosis and autophagy through SPl-dependent mechanisms.
机译：调查是否TP53-induced糖酵解和细胞凋亡调节器(TIGAR)参与compression-induced椎间盘(试管)变性,确定监管TIGAR对髓核细胞(NP)自噬和凋亡compression-induced受伤。从人类收集患者接受手术(n = 20)和Sprague-Dawley只是成熟老鼠(n = 15)。压缩TIGAR的表达上评估体内和体外模型。此外,TIGAR沉默调查compression-induced TIGAR的监管效果细胞内活性氧(ROS)水平,在鼠NP细胞自噬和细胞凋亡。此外,P53抑制剂pifithrin -α(击球α)和了SP1抑制剂光神霉素检测TIGAR和表达水平变化autophagy-associated目标分子。NP细胞的表达逐渐增加人类退化性试管和鼠NP细胞压缩体内和体外。可拆卸的增强compression-induced细胞内ROS生成和NADPH / NADP +与谷胱甘肽(GSSG比率。放大了compression-induced caspase-3激活和鼠NP的细胞凋亡率细胞。加速LC3B表达式和自噬小体在鼠NP细胞形成compression-induced受伤。建立了光神霉素可以抑制TIGAR表达和NP细胞自噬的水平在压缩条件下,而PFTa没有类似的效果。作为一个重要的内生负面监管机构的ROS水平,这可能会抑制compression-induced细胞凋亡和自噬通过SPl-dependent机制。

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