TRPV2 interacts with actin and reorganizes submembranous actin cytoskeleton

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-...

Full description

Saved in:
Bibliographic Details
Published in:Bioscience reports 2020-10, Vol.40 (10)
Main Authors: Yadav, Manoj, Goswami, Chandan
Format: Article
Language:English
Subjects:
Actin Cytoskeleton - metabolism
Actins - metabolism
Animals
Calcium Signaling
Cell Line, Tumor
Cell Membranes, Excitation & Transport
Cell Shape
CHO Cells
Cricetulus
Growth Cones - metabolism
HaCaT Cells
HEK293 Cells
Humans
Neurites - metabolism
Neurogenesis
Neuroscience
Protein Binding
Protein Interaction Domains and Motifs
Time Factors
TRPV Cation Channels - genetics
TRPV Cation Channels - metabolism
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0144-8463
1573-4935
DOI:10.1042/BSR20200118