scholarly journals Sensory Axon Regeneration: A Review from an in vivo Imaging Perspective

2012 ◽  
Vol 21 (3) ◽  
pp. 83-93 ◽  
Author(s):  
Seung Baek Han ◽  
Hyukmin Kim ◽  
Andrew Skuba ◽  
Alan Tessler ◽  
Toby Ferguson ◽  
...  
2016 ◽  
Vol 622 ◽  
pp. 61-66 ◽  
Author(s):  
Yi-Wen Hu ◽  
Jing-Jing Jiang ◽  
Yan-Gao ◽  
Rui-Ying Wang ◽  
Guan-Jun Tu

2011 ◽  
Vol 108 (15) ◽  
pp. 6282-6287 ◽  
Author(s):  
F. M. Bareyre ◽  
N. Garzorz ◽  
C. Lang ◽  
T. Misgeld ◽  
H. Buning ◽  
...  

2018 ◽  
Vol 300 ◽  
pp. 67-73 ◽  
Author(s):  
Bing-bing Hu ◽  
Min Chen ◽  
Rong-chen Huang ◽  
Yu-bin Huang ◽  
Yang Xu ◽  
...  

2020 ◽  
Author(s):  
Qiao Li ◽  
Cheng Qian ◽  
Harry Feng ◽  
Tyger Lin ◽  
Ying Huang ◽  
...  

AbstractRecent studies have shown that DNA N6-methyladenine (N6-mA) modification is emerging to be a novel and important epigenetic regulator of mammalian gene transcription. Several studies demonstrated DNA N6-mA in human or rodents was regulated by methyltransferase N6AMT1 and demethylase ALKBH1. Moreover, studies in mouse brain or human glioblastoma cells showed that reduced level of N6-mA or higher level of ALKBH1 was correlated with up regulated levels of genes associated with neuronal development. We thus investigated the functional roles of ALKBH1 in sensory axon regeneration. Our results showed that ALKBH1 regulated the level of N6-mA in sensory neurons, and upon peripheral nerve injury ALKBH1 was up regulated in mouse sensory neurons. Functionally, knocking down ALKBH1 in sensory neurons resulted in reduced axon regeneration in vitro and in vivo, which could be rescued by simultaneously knocking down N6AMT1. Moreover, knocking down ALKBH1 led to decreased levels of many neurodevelopment regulatory genes, including neuritin that is well known to enhance axon growth and regeneration. Our study not only revealed a novel physiological function of DNA N6-mA, but also identified a new epigenetic mechanism regulating mammalian axon regeneration.Significance StatementThe study demonstrated that DNA N6-methyladenine (N6-mA) modification played important roles in regulation of sensory axon regeneration, likely through controlling the expression of neurodevelopmental associated genes. The results will add new evidence about the physiological function of DNA N6-mA and its regulatory demethylase ALKBH1 in neurons.


2020 ◽  
Vol 15 (6) ◽  
pp. 1160 ◽  
Author(s):  
Feng-Quan Zhou ◽  
Rui-Ying Wang ◽  
Yan Gao ◽  
Yi-Wen Hu ◽  
Run-Shan Duan ◽  
...  

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 808 ◽  
Author(s):  
David Romeo-Guitart ◽  
Caty Casas

Peripheral nerve injury (PNI) leads to the loss of motor, sensory, and autonomic functions, and often triggers neuropathic pain. During the last years, many efforts have focused on finding new therapies to increase axonal regeneration or to alleviate painful conditions. Still only a few of them have targeted both phenomena. Incipient or aberrant sensory axon regeneration is related to abnormal unpleasant sensations, such as hyperalgesia or allodynia. We recently have discovered NeuroHeal, a combination of two repurposed drugs; Acamprosate and Ribavirin. NeuroHeal is a neuroprotective agent that also enhances motor axon regeneration after PNI. In this work, we investigated its effect on sensory fiber regeneration and PNI-induced painful sensations in a rat model of spare nerve injury and nerve crush. The follow up of the animals showed that NeuroHeal treatment reduced the signs of neuropathic pain in both models. Besides, the treatment favored sensory axon regeneration, as observed in dorsal root ganglion explants. Mechanistically, the effects observed in vivo may improve the resolution of cell-protective autophagy. Additionally, NeuroHeal treatment modulated the P2X4-BDNF-KCC2 axis, which is an essential driver of neuropathic pain. These data open a new therapeutic avenue based on autophagic modulation to foster endogenous regenerative mechanisms and reduce the appearance of neuropathic pain in PNI.


2020 ◽  
Vol 48 (6) ◽  
pp. 2657-2667
Author(s):  
Felipe Montecinos-Franjola ◽  
John Y. Lin ◽  
Erik A. Rodriguez

Noninvasive fluorescent imaging requires far-red and near-infrared fluorescent proteins for deeper imaging. Near-infrared light penetrates biological tissue with blood vessels due to low absorbance, scattering, and reflection of light and has a greater signal-to-noise due to less autofluorescence. Far-red and near-infrared fluorescent proteins absorb light >600 nm to expand the color palette for imaging multiple biosensors and noninvasive in vivo imaging. The ideal fluorescent proteins are bright, photobleach minimally, express well in the desired cells, do not oligomerize, and generate or incorporate exogenous fluorophores efficiently. Coral-derived red fluorescent proteins require oxygen for fluorophore formation and release two hydrogen peroxide molecules. New fluorescent proteins based on phytochrome and phycobiliproteins use biliverdin IXα as fluorophores, do not require oxygen for maturation to image anaerobic organisms and tumor core, and do not generate hydrogen peroxide. The small Ultra-Red Fluorescent Protein (smURFP) was evolved from a cyanobacterial phycobiliprotein to covalently attach biliverdin as an exogenous fluorophore. The small Ultra-Red Fluorescent Protein is biophysically as bright as the enhanced green fluorescent protein, is exceptionally photostable, used for biosensor development, and visible in living mice. Novel applications of smURFP include in vitro protein diagnostics with attomolar (10−18 M) sensitivity, encapsulation in viral particles, and fluorescent protein nanoparticles. However, the availability of biliverdin limits the fluorescence of biliverdin-attaching fluorescent proteins; hence, extra biliverdin is needed to enhance brightness. New methods for improved biliverdin bioavailability are necessary to develop improved bright far-red and near-infrared fluorescent proteins for noninvasive imaging in vivo.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S588-S588
Author(s):  
Vladimir Kepe ◽  
Gregory M Cole ◽  
Jie Liu ◽  
Dorothy G Flood ◽  
Stephen P Trusko ◽  
...  

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