Neural precursor cells contain two types of intermediate filaments (IFs): neurofilaments consisting of three IV type proteins and vimentin belonging to the type III IF proteins that disappear at the later stages of differentiation. The involvement of vimentin in neurogenesis was demonstrated earlier; however, the role of its temporary expression in neurons is not clear. We showed that the vimentin IFs that interacted with mitochondria maintained their membrane potential at the appropriate level, and thus, ensured their proper function. We examined the dependence of the mitochondrial membrane potential on the expression of vimentin in a CAD catecholaminergic neuronal cell line that was actively dividing in full culture media but stopped growing and started developing neurites when the serum was removed. Using the CRISPR Cas9 system to knock out the vimentin gene in these cells, we investigated the impact of this on the mitochondrial membrane potential. Our data show that the deletion of the vimentin IFs led to a decrease in the level of the mitochondrial potential. When the vimentin network in these cells was reconstituted by transfection with a plasmid that encoded human protein, the level of the potential was restored. Interestingly, mutated vimentin with a disrupted mitochondria-binding site had no such effect. Our data point to vimentin as a possible target in some neurological pathologies.

Vimentin is found in progenitor cells and at the early stages of differentiation of almost all neurons, in which it is gradually replaced by neurofilament proteins. An expression of vimentin is also observed during the repair of damaged nerve fibers. Based on the data obtained, a number of studies have suggested an important role of this protein in the processes of neuritogenesis, but what this role is, remains unclear. Using CAD neuroblastoma cells with knockout of vimentin gene, we conducted a comparative study of the processes of neurites formation in these modified cells and in the cells of the original line. The results obtained indicate that vimentin provides effective growth of neurites due to the increased directionality of movement of their growth cones. Deficiency in vimentin leads to the fact that the cells form fewer neurites, and those that have formed, are shorter than those of cells with vimentin. The reason for this lag was that in cells without vimentin, the nerve endings move less directionally, often change direction, and sometimes are simply shorten.

Neural precursor cells contain two types of intermediate filaments (IFs): neurofilaments consisting of three IV type proteins, and vimentin belonging to the III type of IF proteins that disappears on the later stages of differentiation. The involvement of vimentin in neurogenesis was demonstrated earlier, however the role of its temporary expression in neurons is not clear. We have shown that vimentin IFs interacting with mitochondria maintain their membrane potential on the appropriate level and thus ensure their proper function. We examined the dependence of mitochondrial membrane potential on the expression of vimentin in CAD catecholaminergic neuronal cell line that is actively dividing in the full culture media but stop growing and start developing neurites when serum is removed. Using CRIPR Cas9 system to knockout the vimentin gene in these cells we investigated the impact of this on the mitochondrial membrane potential. Our data show that deletion of vimentin IFs leads to decrease of the level of mitochondrial potential. When the vimentin network in these cells was reconstituted by transfection with plasmid encoding human protein the level of potential restored. Interestingly, mutated vimentin with disrupted mitochondria-binding site had no such an effect. Our data point to vimentin as a possible target in some neurological pathologies.

Neurons achieve their highly polarized architecture by coordinating cytoskeletal systems across space and time, enabling axons to extend over remarkable distances and dendrites to elaborate complex arbours. Early neuroanatomists described intracellular “neurofibrils,” yet these structures remained poorly understood until electron microscopy resolved them into three distinct polymer systems: microtubules, actin filaments, and intermediate filaments. Although this framework clarified neuronal ultrastructure, it simultaneously established a conceptual hierarchy in which microtubules and actin were regarded as the principal drivers of neurite growth, while intermediate filaments were relegated to a passive, supportive role. Unlike prior reviews that document vimentin dynamics primarily from a cell-biological standpoint, this review integrates historical, conceptual, and epistemological perspectives to examine both how and why that hierarchy arose and how it has been dismantled. This review traces how that hierarchy arose and why it has been increasingly reconsidered in favour of intermediate filaments, focusing on vimentin as a case study. Evidence from live cell imaging, molecular manipulation, and genetic models shows that vimentin is dynamically regulated rather than static. Vimentin networks remodel continuously, exchange subunits with soluble pools, and move in coordination with microtubules. Most recently, sparse single-filament labelling combined with correlative volume electron microscopy has demonstrated that individual vimentin filaments remain motile even within dense perinuclear networks previously assumed to be static, a finding that fundamentally redefines what filament density implies about cytoskeletal organization. In neural and neural precursor cells, vimentin expression is developmentally regulated and is prominent during early differentiation stages associated with neurite initiation giving way to neurofilaments in mature neurons. Functional studies further link vimentin to neurite formation and extension, cytoskeletal coordination, organelle positioning, and cellular stress responses. Philosophical analysis reveals that these empirical advances were inseparable from shifts in imaging technology and conceptual framing, and that epistemic risks including model dependency and confirmation bias can be mitigated through methodological pluralism and explicit model disclosure. Taken together, these findings support a revised understanding of intermediate filaments as active, context-dependent contributors to neuronal development and plasticity, and illustrate the value of integrating biological evidence with historical and philosophical reflection.