scholarly journals Metabolic reprogramming of glial cells as a new target for central nervous system axon regeneration

2022 ◽  
Vol 17 (5) ◽  
pp. 997
Author(s):  
Shuxin Li ◽  
ErinL Walden
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells ◽  
Axon Regeneration ◽  
Metabolic Reprogramming

Neural Stem Cells to Glial Cells an Important Factor for Brain Injury

2020 ◽  
Author(s):  
Prithiv K R Kumar
Keyword(s):  
Stem Cells ◽  
Central Nervous System ◽  
Nervous System ◽  
Neural Stem Cells ◽  
Glial Cells ◽  
Brain Injuries ◽  
The Body ◽  
The Central Nervous System ◽  
Near Future

Stem cells have the capacity to differentiate into any type of cell or organ. Stems cell originate from any part of the body, including the brain. Brain cells or rather neural stem cells have the capacitive advantage of differentiating into the central nervous system leading to the formation of neurons and glial cells. Neural stem cells should have a source by editing DNA, or by mixings chemical enzymes of iPSCs. By this method, a limitless number of neuron stem cells can be obtained. Increase in supply of NSCs help in repairing glial cells which in-turn heal the central nervous system. Generally, brain injuries cause motor and sensory deficits leading to stroke. With all trials from novel therapeutic methods to enhanced rehabilitation time, the economy and quality of life is suppressed. Only PSCs have proven effective for grafting cells into NSCs. Neurons derived from stem cells is the only challenge that limits in-vitro usage in the near future.

scholarly journals Murine Esophagus Expresses Glial-Derived Central Nervous System Antigens

2021 ◽  
Vol 22 (6) ◽  
pp. 3233
Author(s):  
Christopher Kapitza ◽  
Rittika Chunder ◽  
Anja Scheller ◽  
Katherine S. Given ◽  
Wendy B. Macklin ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Schwann Cells ◽  
Glial Cells ◽  
Proteolipid Protein ◽  
Pcr Analysis ◽  
Specific Expression ◽  
Enteric Glial Cells ◽  
Cell Type Specific Expression ◽  
Long Time

Multiple sclerosis (MS) has been considered to specifically affect the central nervous system (CNS) for a long time. As autonomic dysfunction including dysphagia can occur as accompanying phenomena in patients, the enteric nervous system has been attracting increasing attention over the past years. The aim of this study was to identify glial and myelin markers as potential target structures for autoimmune processes in the esophagus. RT-PCR analysis revealed glial fibrillary acidic protein (GFAP), proteolipid protein (PLP), and myelin basic protein (MBP) expression, but an absence of myelin oligodendrocyte glycoprotein (MOG) in the murine esophagus. Selected immunohistochemistry for GFAP, PLP, and MBP including transgenic mice with cell-type specific expression of PLP and GFAP supported these results by detection of (1) GFAP, PLP, and MBP in Schwann cells in skeletal muscle and esophagus; (2) GFAP, PLP, but no MBP in perisynaptic Schwann cells of skeletal and esophageal motor endplates; (3) GFAP and PLP, but no MBP in glial cells surrounding esophageal myenteric neurons; and (4) PLP, but no GFAP and MBP in enteric glial cells forming a network in the esophagus. Our results pave the way for further investigations regarding the involvement of esophageal glial cells in the pathogenesis of dysphagia in MS.

Multifunctionalized Electrospun Silk Fibers Promote Axon Regeneration in the Central Nervous System

2011 ◽  
Vol 21 (22) ◽  
pp. 4232-4242 ◽  
Author(s):  
Corinne R. Wittmer ◽  
Thomas Claudepierre ◽  
Michael Reber ◽  
Peter Wiedemann ◽  
Jonathan A. Garlick ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Axon Regeneration ◽  
Silk Fibers ◽  
The Central Nervous System

scholarly journals MeCP2 in central nervous system glial cells: current updates

2018 ◽  
Vol 78 (1) ◽  
pp. 30-40 ◽  
Author(s):  
Kedarlal Sharma ◽  
Juhi Singh ◽  
Emma E. Frost ◽  
Prakash P. Pillai
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glial Cells

scholarly journals mTORC1 is necessary but mTORC2 and GSK3β are inhibitory for AKT3-induced axon regeneration in the central nervous system

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Linqing Miao ◽  
Liu Yang ◽  
Haoliang Huang ◽  
Feisi Liang ◽  
Chen Ling ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Axon Regeneration ◽  
Nodal Point ◽  
Mtor Signaling ◽  
Negative Regulator ◽  
Molecular Dissection ◽  
Parallel Pathways ◽  
Downstream Effectors ◽  
The Central Nervous System

Injured mature CNS axons do not regenerate in mammals. Deletion of PTEN, the negative regulator of PI3K, induces CNS axon regeneration through the activation of PI3K-mTOR signaling. We have conducted an extensive molecular dissection of the cross-regulating mechanisms in axon regeneration that involve the downstream effectors of PI3K, AKT and the two mTOR complexes (mTORC1 and mTORC2). We found that the predominant AKT isoform in CNS, AKT3, induces much more robust axon regeneration than AKT1 and that activation of mTORC1 and inhibition of GSK3β are two critical parallel pathways for AKT-induced axon regeneration. Surprisingly, phosphorylation of T308 and S473 of AKT play opposite roles in GSK3β phosphorylation and inhibition, by which mTORC2 and pAKT-S473 negatively regulate axon regeneration. Thus, our study revealed a complex neuron-intrinsic balancing mechanism involving AKT as the nodal point of PI3K, mTORC1/2 and GSK3β that coordinates both positive and negative cues to regulate adult CNS axon regeneration.

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