Faculty Opinions recommendation of Metabolic control of sensory neuron survival by the p75 neurotrophin receptor in Schwann cells.

Author(s):  
Mark Bothwell
2021 ◽  
pp. JN-RM-3243-20
Author(s):  
Rose M. Follis ◽  
Chhavy Tep ◽  
Thiago C. Genaro-Mattos ◽  
Mi Lyang Kim ◽  
Jae Cheon Ryu ◽  
...  

Neuron ◽  
2016 ◽  
Vol 90 (6) ◽  
pp. 1215-1229 ◽  
Author(s):  
Yosuke Tanaka ◽  
Shinsuke Niwa ◽  
Ming Dong ◽  
Atena Farkhondeh ◽  
Li Wang ◽  
...  

2018 ◽  
Vol 55 (6) ◽  
pp. 786-801 ◽  
Author(s):  
Kathrin Becker ◽  
Armend Cana ◽  
Wolfgang Baumgärtner ◽  
Ingo Spitzbarth

The low-affinity nerve growth factor receptor p75NTR is a major neurotrophin receptor involved in manifold and pleiotropic functions in the developing and adult central nervous system (CNS). Although known for decades, its entire functions are far from being fully elucidated. Depending on the complex interactions with other receptors and on the cellular context, p75NTR is capable of performing contradictory tasks such as mediating cell death as well as cell survival. In parallel, as a prototype marker for certain differentiation stages of Schwann cells and related CNS aldynoglial cells, p75NTR has recently gained increasing notice as a marker for cells with proposed regenerative potential in CNS diseases, such as demyelinating disease and traumatic CNS injury. Besides its pivotal role as a marker for transplantation candidate cells, recent studies in canine neuroinflammatory CNS conditions also highlight a spontaneous endogenous occurrence of p75NTR-positive glia, which potentially play a role in Schwann cell–mediated CNS remyelination. The aim of the present communication is to review the pleiotropic functions of p75NTR in the CNS with a special emphasis on its role as an immunohistochemical marker in neuropathology. Following a brief illustration of the expression of p75NTR in neurogenesis and in developed neuronal populations, the implications of p75NTR expression in astrocytes, oligodendrocytes, and microglia are addressed. A special focus is put on the role of p75NTR as a cell marker for specific differentiation stages of Schwann cells and a regeneration-promoting CNS population, collectively referred to as aldynoglia.


2020 ◽  
Vol 26 ◽  
Author(s):  
Jun-Jie Tang ◽  
Shuang Feng ◽  
Xing-Dong Chen ◽  
Hua Huang ◽  
Min Mao ◽  
...  

: Neurological diseases bring great mental and physical torture to the patients, and have long-term and sustained negative effects on families and society. The attention to neurological diseases is increasing, and the improvement of the material level is accompanied by an increase in the demand for mental level. The p75 neurotrophin receptor (p75NTR) is a low-affinity neurotrophin receptor and involved in diverse and pleiotropic effects in the developmental and adult central nervous system (CNS). Since neurological diseases are usually accompanied by the regression of memory, the pathogenesis of p75NTR also activates and inhibits other signaling pathways, which has a serious impact on the learning and memory of patients. The results of studies shown that p75NTR is associated with LTP/LTD-induced synaptic enhancement and inhibition, suggest that p75NTR may be involved in the progression of synaptic plasticity. And its pro-apoptotic effect is associated with activation of proBDNF and inhibition of proNGF, and TrkA/p75NTR imbalance leads to pro-survival or pro-apoptotic phenomena. It can be inferred that p75NTR mediates apoptosis in the hippocampus and amygdale, which may affect learning and memory behavior. This article mainly discusses the relationship between p75NTR and learning memory and associated mechanisms, which may provide some new ideas for the treatment of neurological diseases.


2021 ◽  
Vol 22 (10) ◽  
pp. 5055
Author(s):  
Catalina Atorrasagasti ◽  
Flavia Piccioni ◽  
Sophia Borowski ◽  
Irene Tirado-González ◽  
Nancy Freitag ◽  
...  

Liver fibrosis results from many chronic injuries and may often progress to cirrhosis and hepatocellular carcinoma (HCC). In fact, up to 90% of HCC arise in a cirrhotic liver. Conversely, stress is implicated in liver damage, worsening disease outcome. Hence, stress could play a role in disrupting liver homeostasis, a concept that has not been fully explored. Here, in a murine model of TAA-induced liver fibrosis we identified nerve growth factor (NGF) to be a crucial regulator of the stress-induced fibrogenesis signaling pathway as it activates its receptor p75 neurotrophin receptor (p75NTR), increasing liver damage. Additionally, blocking the NGF decreased liver fibrosis whereas treatment with recombinant NGF accelerated the fibrotic process to a similar extent than stress challenge. We further show that the fibrogenesis induced by stress is characterized by specific changes in the hepatoglycocode (increased β1,6GlcNAc-branched complex N-glycans and decreased core 1 O-glycans expression) which are also observed in patients with advanced fibrosis compared to patients with a low level of fibrosis. Our study facilitates an understanding of stress-induced liver injury and identify NGF signaling pathway in early stages of the disease, which contributes to the established fibrogenesis.


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