Functions and the related signaling pathways of the neurotrophic factor neuritin

Yao, Jinjing; Zhao, Qi; Lu, Jing; Mei, Yan‐Ai

doi:10.1038/aps.2017.197

Cited by 34 publications

(25 citation statements)

References 62 publications

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“…The neuroprotective effect of ATF3 overexpression was similar to that of neuritin, a known RGC neuroprotective factor. 7,53 However, a single rAAV-ATF3 injection was not sufficient for RGC neuroprotection over 6 weeks. This indicates that ATF3 effects on injured RGCs may be transient or that multiple rAAV-ATF3 injections are needed, similar to a rat glaucoma model where RGC neuroprotection by intravitreal injections of small extracellular vesicles required monthly injections while a single injection was not effective over 2 months.…”

Section: Discussionmentioning

confidence: 99%

“…For example, it has been shown that optic nerve injury triggers rapid upregulation of the stress-induced proteins REDD1 and REDD2 (regulated in development and DNA damage responses 1 and 2, respectively), potent inhibitors of mTOR. 53,54 REDD2 upregulation and mTOR inhibition led to RGC dendrite pathology causing neuronal dysfunction and subsequent RGC death, 60 whereas suppression of REDD1 expression promoted RGC survival and axon elongation after ONC. 61 Combinatorial action of REDD1/2, PTEN, ATF3, and some other factors may lead to the observed effects.…”

Section: Discussionmentioning

confidence: 99%

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Activating Transcription Factor 3 (ATF3) Protects Retinal Ganglion Cells and Promotes Functional Preservation After Optic Nerve Crush

Kole

Brommer

Nakaya

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To investigate the possible role of activating transcription factor 3 (ATF3) in retinal ganglion cell (RGC) neuroprotection and optic nerve regeneration after optic nerve crush (ONC). METHODS.Overexpression of proteins of interest (ATF3, phosphatase and tensin homolog [PTEN], placental alkaline phosphatase, green fluorescent protein) in the retina was achieved by intravitreal injections of recombinant adenovirus-associated viruses (rAAVs) expressing corresponding proteins. The number of RGCs and αRGCs was evaluated by immunostaining retinal sections and whole-mount retinas with antibodies against RNA binding protein with multiple splicing (RBPMS) and osteopontin, respectively. Axonal regeneration was assessed via fluorophore-coupled cholera toxin subunit B labeling. RGC function was evaluated by recording positive scotopic threshold response. RESULTS.The level of ATF3 is preferentially elevated in osteopontin + /RBPMS + αRGCs following ONC. Overexpression of ATF3 by intravitreal injection of rAAV 2 weeks before ONC promoted RBPMS + RGC survival and preserved RGC function as assessed by positive scotopic threshold response recordings 2 weeks after ONC. However, overexpression of ATF3 and simultaneous downregulation of PTEN, a negative regulator of the mTOR pathway, combined with ONC, only moderately promoted short distance RGC axon regeneration (200 μm from the lesion site) but did not provide additional RGC neuroprotection compared with PTEN downregulation alone. CONCLUSIONS.These results reveal a neuroprotective effect of ATF3 in the retina following injury and identify ATF3 as a promising agent for potential treatments of optic neuropathies.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Activating Transcription Factor 3 (ATF3) Protects Retinal Ganglion Cells and Promotes Functional Preservation After Optic Nerve Crush

Kole

Brommer

Nakaya

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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“…For instance, neuritin mRNA was initially identified as having activity-associated transcription and purified neuritin and was later revealed as a modulator of neurite outgrowth and arborization in embryonic hippocampal and cortical mouse neurons (Naeve et al, 1997 ). Subsequent studies have demonstrated that neuritin induces neuritogenesis and that it plays a role in the maturation and stability of synapses while also increasing neurotransmitter release in cortical neurons (Yao et al, 2018 ). Neuritin activity can also be mediated through nuclear factor of activated T-cells cytoplasmic 4 (NFATc4) and calcineurin (CaN).…”

Section: Mechanisms Of Neuronal Activity-associated Plasticitymentioning

confidence: 99%

Neural Stimulation and Molecular Mechanisms of Plasticity and Regeneration: A Review

Hogan

Hamilton

Horner

2020

Front. Cell. Neurosci.

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Neural stimulation modulates the depolarization of neurons, thereby triggering activity-associated mechanisms of neuronal plasticity. Activity-associated mechanisms in turn play a major role in post-mitotic structure and function of adult neurons. Our understanding of the interactions between neuronal behavior, patterns of neural activity, and the surrounding environment is evolving at a rapid pace. Brain derived neurotrophic factor is a critical mediator of activity-associated plasticity, while multiple immediate early genes mediate plasticity of neurons following bouts of neural activity. New research has uncovered genetic mechanisms that govern the expression of DNA following changes in neural activity patterns, including RNAPII pause-release and activity-associated double stranded breaks. Discovery of novel mechanisms governing activity-associated plasticity of neurons hints at a layered and complex molecular control of neuronal response to depolarization. Importantly, patterns of depolarization in neurons are shown to be important mediators of genetic expression patterns and molecular responses. More research is needed to fully uncover the molecular response of different types of neurons-to-activity patterns; however, known responses might be leveraged to facilitate recovery after neural damage. Physical rehabilitation through passive or active exercise modulates neurotrophic factor expression in the brain and spinal cord and can initiate cortical plasticity commensurate with functional recovery. Rehabilitation likely relies on activity-associated mechanisms; however, it may be limited in its application. Electrical and magnetic stimulation direct specific activity patterns not accessible through passive or active exercise and work synergistically to improve standing, walking, and forelimb use after injury. Here, we review emerging concepts in the molecular mechanisms of activity-derived plasticity in order to highlight opportunities that could add value to therapeutic protocols for promoting recovery of function after trauma, disease, or age-related functional decline.

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“…For the other genes that we detect, Hek et al [43] reports that SNP rs161645 near NUDT12 is associated with depressive symptoms; NRN1L expresses predominantly in the nervous system [44] and may play a role in psychiatric diseases [45]; and STRA13 may have an effect on SCZ by influencing gene CHRNA7 [46].…”

Section: Real Data Applicationmentioning

confidence: 79%

Adaptive Fisher method detects dense and sparse signals in association analysis of SNV sets

et al. 2020

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Background: With the development of next generation sequencing (NGS) technology and genotype imputation methods, statistical methods have been proposed to test a set of genomic variants together to detect if any of them is associated with the phenotype or disease. In practice, within the set, there is an unknown proportion of variants truly causal or associated with the disease. There is a demand for statistical methods with high power in both dense and sparse scenarios, where the proportion of causal or associated variants is large or small respectively. Results: We propose a new association test-weighted Adaptive Fisher (wAF) that can adapt to both dense and sparse scenarios by adding weights to the Adaptive Fisher (AF) method we developed before. Using simulation, we show that wAF enjoys comparable or better power to popular methods such as sequence kernel association tests (SKAT and SKAT-O) and adaptive SPU (aSPU) test. We apply wAF to a publicly available schizophrenia dataset, and successfully detect thirteen genes. Among them, three genes are supported by existing literature; six are plausible as they either relate to other neurological diseases or have relevant biological functions. Conclusions: The proposed wAF method is a powerful disease-variants association test in both dense and sparse scenarios. Both simulation studies and real data analysis indicate the potential of wAF for new biological findings.

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Functions and the related signaling pathways of the neurotrophic factor neuritin

Cited by 34 publications

References 62 publications

Activating Transcription Factor 3 (ATF3) Protects Retinal Ganglion Cells and Promotes Functional Preservation After Optic Nerve Crush

Activating Transcription Factor 3 (ATF3) Protects Retinal Ganglion Cells and Promotes Functional Preservation After Optic Nerve Crush

Neural Stimulation and Molecular Mechanisms of Plasticity and Regeneration: A Review

Adaptive Fisher method detects dense and sparse signals in association analysis of SNV sets

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