Filamin A Is Required in Injured Axons for HDAC5 Activity and Axon Regeneration

Cho, Yongcheol; Park, Dongeun; Cavalli, Valeria

doi:10.1074/jbc.m115.638445

Cited by 21 publications

(15 citation statements)

References 52 publications

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“…PKA then activates dual leucine zipper-bearing kinase (DLK), a key mediator of later regenerative events 34 . Similarly, calcium at the injury site facilitates both the local translation of signal transducer and activator of transcription 3 (STAT3) 57 , importin-β 58 and filamin A 247 , and the association of extracellular-signal-related kinase (ERK) with importin-β, which allows them to be retrogradely transported 52 . The backpropagation of calcium to the cell soma promotes the translocation of serine/ threonine-protein kinase D1 (PRKD1) to the nucleus, which promotes histone deacetylase 5 (HDAC5) nuclear export 20 .…”

Section: Figmentioning

confidence: 99%

“…ERK, which is protected by vimentin during its retrograde transport, causes the histone acetyltransferase KAT2B to translocate into the nucleus 52,166 . Conversely, HDAC5 and HDAC3 are exported from the nucleus in response to PRKD1 nuclear translocation 20 and HDAC5 is transported to the growth cone, where it interacts with filamin A and PRKD1 to deacetylate microtubules 167,247 . The changes in subcellular location of these histone modifiers, along with the calcium-dependent increase in TET3 (REF.…”

Section: Figmentioning

confidence: 99%

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Intrinsic mechanisms of neuronal axon regeneration

2018

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Permanent disabilities following CNS injuries result from the failure of injured axons to regenerate and rebuild functional connections with their original targets. By contrast, injury to peripheral nerves is followed by robust regeneration, which can lead to recovery of sensory and motor functions. This regenerative response requires the induction of widespread transcriptional and epigenetic changes in injured neurons. Considerable progress has been made in recent years in understanding how peripheral axon injury elicits these widespread changes through the coordinated actions of transcription factors, epigenetic modifiers and, to a lesser extent, microRNAs. Although many questions remain about the interplay between these mechanisms, these new findings provide important insights into the pivotal role of coordinated gene expression and chromatin remodelling in the neuronal response to injury.

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Section: Figmentioning

confidence: 99%

Section: Figmentioning

confidence: 99%

Intrinsic mechanisms of neuronal axon regeneration

2018

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“…Growth cone behav-iors are driven by the dynamic reorganization of actin, which in turn is modulated by a number of actin-binding proteins that affect how actin networks are assembled, organized, and remodeled. In particular, actin-binding proteins act as important regulators of axon regeneration by stabilizing filamentous (F) actin (Cho et al, 2015;Tan et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

The C. elegans BRCA2-ALP/Enigma Complex Regulates Axon Regeneration via a Rho GTPase-ROCK-MLC Phosphorylation Pathway

et al. 2018

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The ability of specific neurons to regenerate their axons after injury is governed by cell-intrinsic regeneration pathways. However, the mechanisms regulating axon regeneration are not well understood. Here, we identify the brc-2 gene encoding a homolog of the mammalian BRCA2 tumor suppressor as a regulator of axon regeneration in Caenorhabditis elegans motor neurons. We show that the RHO-1/Rho GTPase-LET-502/ROCK (Rho-associated coiled-coil kinase)-regulatory non-muscle myosin light-chain (MLC-4/MLC) phosphorylation signaling pathway regulates axon regeneration. BRC-2 functions between RHO-1 and LET-502, suggesting that BRC-2 is required for the activation of LET-502 by RHO-1-GTP. We also find that one component that interacts with BRC-2, the ALP (α-actinin-associated LIM protein)/Enigma protein ALP-1, is required for regeneration and acts between LET-502 and MLC-4 phosphorylation. Furthermore, we demonstrate that ALP-1 associates with LET-502 and MLC-4. Thus, ALP-1 serves as a platform to activate MLC-4 phosphorylation mediated by the RHO-1-LET-502 signaling pathway.

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“…Because acetylated tubulin is enriched in stable microtubules, activation of histone deacetylase 5 (HDAC5), which is activated by calcium ions, accelerates microtubule depolymerization through tubulin deacetylation. (48,49) Nitrated alpha-tubulin levels are correlated with microtubule stabilization in PC12 cells. (50) Although these studies, including our previous reports, implicate ROS-derived microtubule dysfunction in axonal degeneration, a detailed correlation between ROS levels and microtubule disruption is not fully understood.…”

Section: Ros Treatment Induces Membrane Oxidation Microtubule Destabmentioning

confidence: 99%

Reactive oxygen species induce neurite degeneration before induction of cell death

Fukui

2016

J. Clin. Biochem. Nutr.

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Reactive oxygen species (ROS) induce neuronal cell death in a time- and concentration-dependent manner. Treatment of cultured cells with a low concentration of hydrogen peroxide induces neurite degeneration, but not cell death. Neurites (axons and dendrites) are vulnerable to ROS. Neurite degeneration (shrinkage, accumulation, and fragmentation) has been found in neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease. However, the mechanism of ROS-related neurite degeneration is not fully understood. Many studies have demonstrated the relationship between mitochondrial dysfunction and microtubule destabilization. These dysfunctions are deeply related to changes in calcium homeostasis and ROS production in neurites. Treatment with antioxidant substances, such as vitamin E, prevents neurite degeneration in cultured cells. This review describes the possibility that ROS induces neurite degeneration before the induction of cell death.

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Filamin A Is Required in Injured Axons for HDAC5 Activity and Axon Regeneration

Cited by 21 publications

References 52 publications

Intrinsic mechanisms of neuronal axon regeneration

Intrinsic mechanisms of neuronal axon regeneration

The C. elegans BRCA2-ALP/Enigma Complex Regulates Axon Regeneration via a Rho GTPase-ROCK-MLC Phosphorylation Pathway

Reactive oxygen species induce neurite degeneration before induction of cell death

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