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Nerve growth factor-mediated paracrine regulation of hepatic stellate cells by multipotent mesenchymal stromal cells.

机译：神经生长因子介导的多能间充质基质细胞对肝星状细胞的旁分泌调节。

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AIMS: Multipotent mesenchymal stromal cells (MSC) have been reported to prevent the development of liver fibrosis and have emerged as a promising strategy for cell-based therapy. However, the underlying therapeutic mechanism remains unclear. Hepatic stellate cells (SC) activation is a pivotal event in the development of liver fibrosis. MAIN METHODS: We hypothesized that MSC play an important role in regulating SC proliferation and apoptosis through paracrine mechanisms. To investigate the paracrine interactions between MSC and SC, a co-culture experimental model was developed using human MSC (hMSC) and human SC (hSC). KEY FINDINGS: We demonstrate that hMSC and hSC both express nerve growth factor (NGF) receptor p75. Results acquired from transwell co-culture experiments using hSC and hMSC showed that hMSC secrete NGF, which enhances hSC apoptosis. Transcription factor nuclear factor kappa B (NF-KappaB) and B cell leukemia-xl (Bcl-xl) take part in the process. SIGNIFICANCE: These findings demonstrated that hMSC indirectly modulate activated hSC in vitro via NGF-mediated signaling cascades and provide a potential mechanism of how transplanted MSC are effective in treating liver fibrosis.
机译：目的：据报道多能间充质基质细胞（MSC）可以预防肝纤维化的发展，并已成为基于细胞疗法的一种有前途的策略。但是，基本的治疗机制仍不清楚。肝星状细胞（SC）激活是肝纤维化发展中的关键事件。主要方法：我们假设MSC通过旁分泌机制在调节SC增殖和凋亡中起重要作用。为了研究MSC和SC之间的旁分泌相互作用，使用人MSC（hMSC）和人SC（hSC）建立了共培养实验模型。主要发现：我们证明hMSC和hSC都表达神经生长因子（NGF）受体p75。从使用hSC和hMSC的跨孔共培养实验获得的结果表明，hMSC分泌NGF，从而增强hSC的细胞凋亡。转录因子核因子κB（NF-KappaB）和B细胞白血病-xl（Bcl-xl）参与了该过程。意义：这些发现表明，hMSC通过NGF介导的信号级联反应间接地在体外调节活化的hSC，并提供了一种潜在的机制，说明移植的MSC如何有效治疗肝纤维化。

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