EEF1A1 deacetylation enables transcriptional activation of remyelination

Duman, Mert; Vaquié, Adrien; Nocera, Gianluigi; Heller, Manfred; Stumpe, Michael; Sankar, Devanarayanan Siva; Dengjel, Jörn; Meijer, Dies; Yamaguchi, Teppei; Matthias, Patrick; Zeis, Thomas; Schaeren‐Wiemers, Nicole; Hayoz, Antoinette; Ruff, Sophie; Jacob, Claire

doi:10.1038/s41467-020-17243-z

Cited by 38 publications

(43 citation statements)

References 72 publications

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“…**p < 0.01 vs Control siRNA group. that the eEF1A1 protein may have therapeutic relevance in diverse conditions with altered neurite outgrowth (McLachlan et al, 2019;Duman et al, 2020). A recent study has suggested that eEF1A1 and CagA cooperated to mediate the expression of IL-6 by affecting the activity of p-STATS727 in the nucleus (Xu et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

MLIF Modulates Microglia Polarization in Ischemic Stroke by Targeting eEF1A1

et al. 2021

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Monocyte locomotion inhibitory factor (MLIF) is a heat-stable pentapeptide from Entamoeba histolytica. Our previous study found that MLIF protects against ischemic stroke in rats and mice and exerts a neuroprotection effect in human neuroblastoma SH-SY5Y cells. Microglia/macrophage polarization has been proven to be vital in the pathology of ischemic stroke. Nevertheless, whether MLIF is able to modulate microglia/macrophage polarization remains unclear. We performed middle cerebral artery occlusion (MCAO) on C57BL/6J male mice and induced cultured BV2 microglia by oxygen-glucose deprivation (OGD), respectively. Immunfluorescence was utilized to detect the M1/2 markers, such as CD206 and CD16/32. qPCR and ELISA were used to detect the signature gene change of M1/2. The MAPK and NF-κB pathway associated proteins were measured by Western blot. To identify the protein target of MLIF, a pull-down assay was performed. We found that MLIF promoted microglia transferring from a “sick” M1 phenotype to a “healthy” M2 phenotype in vivo or in vitro. Furthermore, we proved that eukaryotic elongation factor 1A1 (eEF1A1) was involved in the modulation of microglia/macrophage polarization. Knocking down eEF1A1 by siRNA exhibited the M1 promotion effect and M2 inhibition effect. Taken together, our results demonstrated MLIF modulated microglia/macrophage polarization by targeting eEF1A1 in ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

MLIF Modulates Microglia Polarization in Ischemic Stroke by Targeting eEF1A1

et al. 2021

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“…It will be important to determine if such biases also exist in cranial neural crest and if different SoxE factors play roles in establishing these predispositions. In addition, there is evidence for direct interaction of Sox factors with epigenetic factors, such as HDACs, to regulate cell fate decisions (Duman et al, 2020). To date, studies of Sox partners/co-factors have predominately focused on other transcription factors.…”

Section: Discussionmentioning

confidence: 99%

“…Regulation of Sox10 in Schwann cells has been linked with eEF1A1 which, upon acetylation, removes SOX10 from the nucleus. In Schwann cells, this activity is blocked by HDAC1/2, Sox10 co-factors essential for myelination, which deacetylate eEF1A1 causing it to return to the cytoplasm and preventing nuclear export of Sox10 (Duman et al, 2020). Finally, one of the essential functions of Sox10 is to direct the neuroglial progenitor cells of the DRG toward the glial lineage.…”

Section: Sox Factors and The Peripheral Nervous Systemmentioning

confidence: 99%

Sorting Sox: Diverse Roles for Sox Transcription Factors During Neural Crest and Craniofacial Development

Schock

LaBonne

2020

Front. Physiol.

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Sox transcription factors play many diverse roles during development, including regulating stem cell states, directing differentiation, and influencing the local chromatin landscape. Of the twenty vertebrate Sox factors, several play critical roles in the development the neural crest, a key vertebrate innovation, and the subsequent formation of neural crest-derived structures, including the craniofacial complex. Herein, we review the specific roles for individual Sox factors during neural crest cell formation and discuss how some factors may have been essential for the evolution of the neural crest. Additionally, we describe how Sox factors direct neural crest cell differentiation into diverse lineages such as melanocytes, glia, and cartilage and detail their involvement in the development of specific craniofacial structures. Finally, we highlight several SOXopathies associated with craniofacial phenotypes.

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“…A more recent study by Duman et al discovered that theophylline enhanced CNS and PNS remyelination by increasing HDAC2, SOX10 and MBP protein levels in young adults and old mice after inducing a focal demyelinating lesion in the spinal cord. The increased remyelination efficiency of theophylline only occurred in the lesion site [ 77 ]. Ruiz-Perera et al also discovered a potential link between methylxanthines and MS.…”

Section: Multiple Sclerosismentioning

confidence: 99%

Methylxanthines and Neurodegenerative Diseases: An Update

et al. 2021

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Methylxanthines (MTX) are purine derived xanthine derivatives. Whereas naturally occurring methylxanthines like caffeine, theophylline or theobromine are widely consumed in food, several synthetic but also non-synthetic methylxanthines are used as pharmaceuticals, in particular in treating airway constrictions. Besides the well-established bronchoprotective effects, methylxanthines are also known to have anti-inflammatory and anti-oxidative properties, mediate changes in lipid homeostasis and have neuroprotective effects. Known molecular mechanisms include adenosine receptor antagonism, phosphodiesterase inhibition, effects on the cholinergic system, wnt signaling, histone deacetylase activation and gene regulation. By affecting several pathways associated with neurodegenerative diseases via different pleiotropic mechanisms and due to its moderate side effects, intake of methylxanthines have been suggested to be an interesting approach in dealing with neurodegeneration. Especially in the past years, the impact of methylxanthines in neurodegenerative diseases has been extensively studied and several new aspects have been elucidated. In this review we summarize the findings of methylxanthines linked to Alzheimer´s disease, Parkinson’s disease and Multiple Sclerosis since 2017, focusing on epidemiological and clinical studies and addressing the underlying molecular mechanisms in cell culture experiments and animal studies in order to assess the neuroprotective potential of methylxanthines in these diseases.

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EEF1A1 deacetylation enables transcriptional activation of remyelination

Cited by 38 publications

References 72 publications

MLIF Modulates Microglia Polarization in Ischemic Stroke by Targeting eEF1A1

MLIF Modulates Microglia Polarization in Ischemic Stroke by Targeting eEF1A1

Sorting Sox: Diverse Roles for Sox Transcription Factors During Neural Crest and Craniofacial Development

Methylxanthines and Neurodegenerative Diseases: An Update

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