Department of Anatomy, School of Basic Medical Sciences, Mudanjiang Medical University, Mudanjiang, Heilongjiang, 157011, China.
Department of Pathology, The First Clinical Medical School of Mudanjiang Medical University, No. 3, Tongxiang Street, Aimin District, Mudanjiang, Heilongjiang, 157011, China.
J Bioenerg Biomembr. 2023 Jun;55(3):195-205. doi: 10.1007/s10863-023-09967-6. Epub 2023 May 27.
Adipose tissue-derived mesenchymal stem cells (ADSCs) have promising effects on nerve repair due to the differentiation ability to neural cells. Ghrelin has been shown to promote the neural differentiation of ADSCs. This work was designed to explore its underlying mechanism. Herein, we found high expression of LNX2 in ADSCs after neuronal differentiation. Knockdown of LNX2 might block neuronal differentiation of ADSCs, as evidenced by the decreased number of neural-like cells and dendrites per cell, and the reduced expressions of neural markers (including β-Tubulin III, Nestin, and MAP2). We also demonstrated that LNX2 silencing suppressed the nuclear translocation of β-catenin in differentiated ADSCs. Luciferase reporter assay indicated that LNX2 inhibited wnt/β-catenin pathway by reducing its transcriptional activity. In addition, results showed that LNX2 expression was increased by ghrelin, and its inhibition diminished the effects of ghrelin on neuronal differentiation. Altogether, the results suggest that LNX2 is involved in the role of ghrelin to facilitate neuronal differentiation of ADSCs.
脂肪组织来源的间充质干细胞（ADSCs）具有向神经细胞分化的能力，因此对神经修复具有良好的效果。胃饥饿素已被证明能促进 ADSCs 的神经分化。本研究旨在探讨其潜在的机制。在此，我们发现神经元分化后的 ADSCs 中 LNX2 表达上调。LNX2 的敲低可能会阻止 ADSCs 的神经分化，这表现在神经样细胞和每个细胞的树突数量减少，以及神经标记物（包括β-Tubulin III、Nestin 和 MAP2）的表达降低。我们还证明，LNX2 沉默抑制了分化后的 ADSCs 中β-catenin 的核易位。荧光素酶报告基因分析表明，LNX2 通过降低其转录活性来抑制 wnt/β-catenin 通路。此外，结果表明，胃饥饿素增加了 LNX2 的表达，而其抑制作用减弱了胃饥饿素对神经元分化的影响。综上所述，这些结果表明，LNX2 参与了胃饥饿素促进 ADSCs 神经元分化的作用。
