Yingying Lin, Xin Wang, Xinyu Cui, Na Zhu, Yanyan Li, Xin Li
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引用次数: 0
Abstract
Vitamin A (VA) and its active form, retinoic acid (RA), are crucial for preserving hepatic stellate cells (HSCs) quiescence and reversing fibrosis. While C6orf120 is known to be involved in HSC activation, its role in RA signaling is unclear. This study found that C6orf120 knockdown markedly reduced CCL4-induced liver fibrosis and TGF-β1-induced activation in LX-2 cells, a human HSC line. This inhibition was associated with enhanced RA signaling, particularly affecting the RA receptor beta (RARβ). Inhibition of RARβ significantly reversed the protective effects of C6orf120 knockdown, indicating that RARβ signaling contributes to the inhibitory effect of C6orf120 knockdown on HSC activation. Our results reveal that C6orf120 inhibition could be a therapeutic strategy for liver fibrosis by regulating RARβ signaling.
维生素 A（VA）及其活性形式--视黄酸（RA）对于维持肝星状细胞（HSCs）静止和逆转纤维化至关重要。众所周知，C6orf120参与了造血干细胞的活化，但它在视黄酸信号转导中的作用尚不清楚。本研究发现，C6orf120的敲除明显减少了CCL4诱导的肝纤维化和TGF-β1诱导的LX-2细胞（一种人类造血干细胞系）的活化。这种抑制作用与 RA 信号转导增强有关，特别是对 RA 受体 beta（RARβ）的影响。抑制RARβ能显著逆转C6orf120敲除的保护作用，表明RARβ信号传导是C6orf120敲除对造血干细胞活化的抑制作用的原因之一。我们的研究结果表明，通过调节RARβ信号传导，抑制C6orf120可能是一种治疗肝纤维化的策略。
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Cell Biochemistry and Biophysics (CBB) aims to publish papers on the nature of the biochemical and biophysical mechanisms underlying the structure, control and function of cellular systems
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