Cofilin 1 activation prevents the defects in axon elongation and guidance induced by extracellular alpha-synuclein

Tilve, Sharada; Difato, Francesco; Chieregatti, Evelina

doi:10.1038/srep16524

Cited by 37 publications

(30 citation statements)

References 44 publications

(52 reference statements)

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“…β‐actin alone is not a direct measure of neuronal injury, and future experiments will understand changes in other structural proteins like Cofilin 1 (Tilve et al . ) in this model. Figure (A–E) shows spinal cord phospholipase protein levels in control mice and mice subjected to EAE that were treated with either water or glyceryl triacetate.…”

Section: Resultsmentioning

confidence: 95%

Increasing acetyl‐CoA metabolism attenuates injury and alters spinal cord lipid content in mice subjected to experimental autoimmune encephalomyelitis

Chevalier

Rosenberger

2017

Journal of Neurochemistry

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Acetate supplementation increases brain acetyl-CoA metabolism, alters histone and non-histone protein acetylation, increases brain energy reserves, and is anti-inflammatory and neuroprotective in rat models of neuroinflammation and neuroborreliosis. To determine the impact acetate supplementation has on a mouse model of multiple sclerosis, we quantified the effect treatment had on injury progression, spinal cord lipid content, phospholipase levels, and myelin structure in mice subjected to experimental autoimmune encephalomyelitis (EAE). EAE was induced by inoculating mice with a myelin oligodendrocyte glycoprotein peptide fragment (MOG ), and acetate supplementation was maintained with 4 g/kg glyceryl triacetate by a daily oral gavage. Acetate supplementation prevented the onset of clinical signs in mice subject to EAE compared to control-treated mice. Furthermore, acetate supplementation prevented the loss of spinal cord ethanolamine and choline glycerophospholipid and phosphatidylserine in mice subjected to EAE compared to EAE animals treated with water. Treatment increased saturated and monounsaturated fatty acid levels in phosphatidylserine compared to controls suggesting that acetate was utilized to increase spinal cord fatty acid content. Also, acetate supplementation prevented the loss of spinal cord cholesterol in EAE animals but did not change cholesteryl esters. Treatment significantly increased GD3 and GD1a ganglioside levels in EAE mice when compared to EAE mice treated with water. Treatment returned levels of phosphorylated and non-phosphorylated cytosolic phospholipase A (cPLA ) levels back to baseline and based on FluoroMyelin™ histochemistry maintained myelin structural characteristics. Overall, these data suggest that acetate supplementation may modulate lipid metabolism in mice subjected to EAE.

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Section: Resultsmentioning

confidence: 95%

Increasing acetyl‐CoA metabolism attenuates injury and alters spinal cord lipid content in mice subjected to experimental autoimmune encephalomyelitis

Chevalier

Rosenberger

2017

Journal of Neurochemistry

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“…), can promote defects in the axon elongation and guidance (Tilve et al . ), as well as in growth and migration in developing neurons (Ronzitti et al . ).…”

Section: Cell Models Based On the Treatment With Exogenous α‐Syn Speciesmentioning

confidence: 99%

In vitro models of synucleinopathies: informing on molecular mechanisms and protective strategies

Marvian

Koss

Aliakbari

et al. 2019

Journal of Neurochemistry

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Alpha‐synuclein (α‐Syn) is a central player in Parkinson's disease (PD) and in a spectrum of neurodegenerative diseases collectively known as synucleinopathies. The protein was first associated with PD just over 20 years ago, when it was found to (i) be a major component of Lewy bodies and (ii) to be also associated with familial forms of PD. The characterization of α‐Syn pathology has been achieved through postmortem studies of human brains. However, the identification of toxic mechanisms associated with α‐Syn was only achieved through the use of experimental models. In vitro models are highly accessible, enable relatively rapid studies, and have been extensively employed to address α‐Syn‐associated neurodegeneration. Given the diversity of models used and the outcomes of the studies, a cumulative and comprehensive perspective emerges as indispensable to pave the way for further investigations. Here, we subdivided in vitro models of α‐Syn pathology into three major types: (i) models simulating α‐Syn fibrillization and the formation of different aggregated structures in vitro, (ii) models based on the intracellular expression of α‐Syn, reporting on pathogenic conditions and cellular dysfunctions induced, and (iii) models using extracellular treatment with α‐Syn aggregated species, reporting on sites of interaction and their downstream consequences. In summary, we review the underlying molecular mechanisms discovered and categorize protective strategies, in order to pave the way for future studies and the identification of effective therapeutic strategies. This article is part of the Special Issue “Synuclein”.

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“…First, actin waves seem to propagate using directional actin treadmilling that generates mechanical force (Katsuno et al, 2015). Actin polymerization and depolymerization is accompanied by the presence of several actin-associated proteins, such as Arp3, cofilin, or shootin within the actin wave (Flynn et al, 2009; Toriyama et al, 2006; Tilve et al, 2015). Interestingly, the wave of actin polymerization directs microtubule-based transport by triggering an upstream wave of microtubule polymerization mediated by a transient widening of the neurite shaft (Winans et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Geometrical Determinants of Neuronal Actin Waves

Tomba

Braïni

Bugnicourt

et al. 2017

Front. Cell. Neurosci.

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Hippocampal neurons produce in their early stages of growth propagative, actin-rich dynamical structures called actin waves. The directional motion of actin waves from the soma to the tip of neuronal extensions has been associated with net forward growth, and ultimately with the specification of neurites into axon and dendrites. Here, geometrical cues are used to control actin wave dynamics by constraining neurons on adhesive stripes of various widths. A key observable, the average time between the production of consecutive actin waves, or mean inter-wave interval (IWI), was identified. It scales with the neurite width, and more precisely with the width of the proximal segment close to the soma. In addition, the IWI is independent of the total number of neurites. These two results suggest a mechanistic model of actin wave production, by which the material conveyed by actin waves is assembled in the soma until it reaches the threshold leading to the initiation and propagation of a new actin wave. Based on these observations, we formulate a predictive theoretical description of actin wave-driven neuronal growth and polarization, which consistently accounts for different sets of experiments.

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Cofilin 1 activation prevents the defects in axon elongation and guidance induced by extracellular alpha-synuclein

Cited by 37 publications

References 44 publications

Increasing acetyl‐CoA metabolism attenuates injury and alters spinal cord lipid content in mice subjected to experimental autoimmune encephalomyelitis

Increasing acetyl‐CoA metabolism attenuates injury and alters spinal cord lipid content in mice subjected to experimental autoimmune encephalomyelitis

In vitro models of synucleinopathies: informing on molecular mechanisms and protective strategies

Geometrical Determinants of Neuronal Actin Waves

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