Abstract
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.
Highlights
Regeneration of neurites, especially in the peripheral tissue, has immense importance in the context of different neuronal disorders
We investigated the expression of transient receptor potential vanilloid 2 (TRPV2) in F11 cells in our culture conditions by immunofluorescence and Western blot analysis
In order to confirm this endogenous expression further, we loaded cells with Fluo-4 AM, a Ca2+-sensor dye and treated these cells with TRPV2-specific agonists and performed live cell imaging to acquire the changes in the Ca2+-level
Summary
Regeneration of neurites, especially in the peripheral tissue, has immense importance in the context of different neuronal disorders. Regulation of membrane proteins and membrane dynamics, vesicular recycling, submembranous cytoskeleton and subsequently basic cytoskeletal reorganization are major events involved. All these events are primarily regulated by an array of regulatory proteins that are present on the cell surface, such as ion channels, receptors and adhesion molecules which sense the different chemical signaling cues and allow the neurons to respond [8,9,10]. Changes in the spatiotemporal Ca2+-levels and Ca2+-oscillation patterns have been correlated with most of these functions [2,8,9,10], which strongly suggest the importance of different Ca2+ channels in the regulation of neuritogenesis. Understanding neuritogenesis at cellular and molecular levels are relevant for several neurological disorders including peripheral neuropathy and neurodegeneration
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