National Institute of Science Education and Research, School of Biological Sciences, Jatni, Khurda 752050, Odisha, India.
Homi Bhabha National Institute, Training School Complex, Anushakti Nagar, Mumbai 400094, India.
Biosci Rep. 2020 Oct 30;40(10). doi: 10.1042/BSR20200118.
The understanding of molecules and their role in neurite initiation and/or extension is not only helpful to prevent different neurodegenerative diseases but also can be important in neuronal damage repair. In this work, we explored the role of transient receptor potential vanilloid 2 (TRPV2), a non-selective cation channel in the context of neurite functions. We confirm that functional TRPV2 is endogenously present in F11 cell line, a model system mimicking peripheral neuron. In F11 cells, TRPV2 localizes in specific subcellular regions enriched with filamentous actin, such as in growth cone, filopodia, lamellipodia and in neurites. TRPV2 regulates actin cytoskeleton and also interacts with soluble actin. Ectopic expression of TRPV2-GFP in F11 cell induces more primary and secondary neurites, confirming its role in neurite initiation, extension and branching events. TRPV2-mediated neuritogenesis is dependent on wildtype TRPV2 as cells expressing TRPV2 mutants reveal no neuritogenesis. These findings are relevant to understand the sprouting of new neurites, neuroregeneration and neuronal plasticity at the cellular, subcellular and molecular levels. Such understanding may have further implications in neurodegeneration and peripheral neuropathy.
对分子及其在轴突起始和/或延伸中的作用的理解不仅有助于预防各种神经退行性疾病，而且对于神经元损伤修复也很重要。在这项工作中，我们探讨了瞬时受体电位香草素 2（TRPV2）在轴突功能方面的作用，TRPV2 是一种非选择性阳离子通道，存在于外周神经元模型系统 F11 细胞系中。在 F11 细胞中，TRPV2 定位于富含丝状肌动蛋白的特定亚细胞区域，如生长锥、丝状伪足、片状伪足和轴突。TRPV2 调节肌动蛋白细胞骨架并与可溶性肌动蛋白相互作用。TRPV2-GFP 的异位表达可诱导 F11 细胞中更多的初级和次级轴突，证实了其在轴突起始、延伸和分支事件中的作用。TRPV2 介导的轴突发生依赖于野生型 TRPV2，因为表达 TRPV2 突变体的细胞不会发生轴突发生。这些发现与理解细胞、亚细胞和分子水平上新轴突的发芽、神经再生和神经元可塑性有关。这种理解可能对神经退行性变和周围神经病有进一步的影响。
