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首页> 外文期刊>Journal of cellular physiology. >IncRNA HOTAIR upregulates autophagy to promote apoptosis and senescence of nucleus pulposus cells
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IncRNA HOTAIR upregulates autophagy to promote apoptosis and senescence of nucleus pulposus cells

机译：IncRNA热空气上调自噬促进髓核细胞凋亡与衰老细胞

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摘要

Intervertebral disc degeneration (IDD) is a complex and chronic disease that involves disc cell senescence, death, and extracellular matrix (ECM) degradation. HOTAIR, a long non-coding RNA (IncRNA) is reportedly associated with autophagy, whereas autophagy is shown to promote IDD. However, how it affects nucleus pulposus (NP) cells, the primary component of intervertebral discs is still unclear. We hypothesized that HOTAIR promotes NP cell apoptosis and senescence through upregulating autophagy. Thus, silencing HOTAIR should inhibit autophagy and exert a therapeutic effect on IDD. Our in vitro experiments in human NP cells revealed that HOTAIR expression positively correlated with IDD grade, and overexpression enhanced autophagy. Autophagy inhibition via 3-methyladenine reversed HOTAIR stimulatory effects on apoptosis, senescence, and ECM catabolism, while the AMP-activated protein kinase (AMPK) inhibitor Compound C suppressed HOTAIR-induced autophagy through regulating AMPK/mTOR/ULK1 pathways. Our in vivo experiment then illustrated that silencing HOTAIR ameliorates IDD in rats. Collectively, we demonstrated that HOTAIR stimulates autophagy to promote NP cell apoptosis, senescence, and ECM catabolism. Therefore, silencing HOTAIR has the potential to become a treatment option for IDD.
机译：椎间盘变性(IDD)复杂的和慢性疾病,涉及光盘细胞衰老、死亡和细胞外基质(ECM)退化。据报道(IncRNA)与自噬,而自噬促进IDD显示。然而,它如何影响髓核(NP)细胞,椎间的主要组件光盘还不清楚。热空气促进NP细胞凋亡和衰老通过上调自噬。热空气应该抑制自噬和发挥对IDD治疗效果。人类NP细胞实验表明热空气表达式和IDD呈正相关级和超表达增强的自噬。自噬抑制通过3-methyladenine逆转热空气刺激对细胞凋亡的影响,和ECM分解代谢,而衰老活化蛋白激酶(AMPK)抑制剂复合C抑制HOTAIR-induced自噬通过调控AMPK / mTOR ULK1通路。体内实验表明沉默的热空气改善IDD的老鼠。总的来说,我们证明了热空气刺激细胞自噬促进NP细胞凋亡、衰老和ECM分解代谢。因此,沉默热空气有潜力成为IDD的治疗选择。

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