scholarly journals Is there a role for the p75 neurotrophin receptor in mediating degeneration during oxidative stress and after hypoxia?

2021 ◽  
Author(s):  
Kornraviya Sankorrakul ◽  
Lei Qian ◽  
Wipawan Thangnipon ◽  
Elizabeth J Coulson
Keyword(s):  
Oxidative Stress ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor

scholarly journals A Role for the p75 Neurotrophin Receptor in Axonal Degeneration and Apoptosis Induced by Oxidative Stress

2014 ◽  
Vol 289 (31) ◽  
pp. 21205-21216 ◽  
Author(s):  
Bradley R. Kraemer ◽  
John P. Snow ◽  
Peter Vollbrecht ◽  
Amrita Pathak ◽  
William M. Valentine ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Axonal Degeneration ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor

The Effects of P75NTR on Learning Memory Mediated by Hippocampal Apoptosis and Synaptic Plasticity

2020 ◽  
Vol 26 ◽  
Author(s):  
Jun-Jie Tang ◽  
Shuang Feng ◽  
Xing-Dong Chen ◽  
Hua Huang ◽  
Min Mao ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Neurological Diseases ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Negative Effects ◽  
Apoptotic Effect ◽  
New Ideas ◽  
The Relationship

: 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.

scholarly journals Acceleration of TAA-Induced Liver Fibrosis by Stress Exposure Is Associated with Upregulation of Nerve Growth Factor and Glycopattern Deviations

2021 ◽  
Vol 22 (10) ◽  
pp. 5055
Author(s):  
Catalina Atorrasagasti ◽  
Flavia Piccioni ◽  
Sophia Borowski ◽  
Irene Tirado-González ◽  
Nancy Freitag ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Liver Damage ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Nerve Growth ◽  
Fibrotic Process ◽  
Ngf Signaling

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.

scholarly journals Cell non-autonomous requirement of p75 in the development of geniculate oral sensory neurons

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Tao Tang ◽  
Christopher R. Donnelly ◽  
Amol A. Shah ◽  
Robert M. Bradley ◽  
Charlotte M. Mistretta ◽  
...  
Keyword(s):  
Sensory Neurons ◽  
Significant Loss ◽  
Taste Buds ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Tactile Stimuli ◽  
Oral Sensory ◽  
Nerve Recordings

AbstractDuring development of the peripheral taste system, oral sensory neurons of the geniculate ganglion project via the chorda tympani nerve to innervate taste buds in fungiform papillae. Germline deletion of the p75 neurotrophin receptor causes dramatic axon guidance and branching deficits, leading to a loss of geniculate neurons. To determine whether the developmental functions of p75 in geniculate neurons are cell autonomous, we deleted p75 specifically in Phox2b + oral sensory neurons (Phox2b-Cre; p75fx/fx) or in neural crest-derived cells (P0-Cre; p75fx/fx) and examined geniculate neuron development. In germline p75−/− mice half of all geniculate neurons were lost. The proportion of Phox2b + neurons, as compared to Phox2b-pinna-projecting neurons, was not altered, indicating that both populations were affected similarly. Chorda tympani nerve recordings demonstrated that p75−/− mice exhibit profound deficits in responses to taste and tactile stimuli. In contrast to p75−/− mice, there was no loss of geniculate neurons in either Phox2b-Cre; p75fx/fx or P0-Cre; p75fx/fx mice. Electrophysiological analyses demonstrated that Phox2b-Cre; p75fx/fx mice had normal taste and oral tactile responses. There was a modest but significant loss of fungiform taste buds in Phox2b-Cre; p75fx/fx mice, although there was not a loss of chemosensory innervation of the remaining fungiform taste buds. Overall, these data suggest that the developmental functions of p75 are largely cell non-autonomous and require p75 expression in other cell types of the chorda tympani circuit.

scholarly journals Erratum: Cerebellar Purkinje cell p75 neurotrophin receptor and autistic behavior

2014 ◽  
Vol 4 (10) ◽  
pp. e476-e476
Author(s):  
L T Lotta ◽  
K Conrad ◽  
D Cory-Slechta ◽  
N F Schor
Keyword(s):  
Purkinje Cell ◽  
Cerebellar Purkinje Cell ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Autistic Behavior

scholarly journals Cornel Iridoid Glycoside Improves Locomotor Impairment and Decreases Spinal Cord Damage in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-12
Author(s):  
Wen-jing Tang ◽  
Deng-lei Ma ◽  
Cui-cui Yang ◽  
Li Zhang ◽  
Ya-li Li ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Rating Scale ◽  
Iridoid Glycoside ◽  
Neurotrophin Receptor ◽  
Intragastric Administration ◽  
P75 Neurotrophin Receptor ◽  
Lesion Site ◽  
Cord Injury ◽  
Locomotor Impairment ◽  
Cornel Iridoid Glycoside

Purpose. This study was to investigate the effects of cornel iridoid glycoside (CIG) on spinal cord injury (SCI) in rats. Methods. The thoracic cord (at T9) of rats was injured by clip compression for 30 sec. Locomotor function was assessed using the Basso, Beattie, and Bresnahan (BBB) rating scale. Neuroanatomic stereological parameters as well as Nogo-A, p75 neurotrophin receptor (p75NTR), and ROCKII expression were measured by histological processing, immunohistochemistry, and stereological analyses. The axons passing through the lesion site were detected by BDA tracing. Results. Intragastric administration of CIG (60 and 180 mg/kg) improved the locomotor impairment at 10, 17, 24, and 31 days post-injury (dpi) compared with untreated SCI model rats. CIG treatment decreased the volume of the lesion epicenter (LEp) and increased the volume of spared tissue and the number of surviving neurons in the injured spinal cord at 31 dpi. CIG promoted the growth of BDA-positive axons and their passage through the lesion site and decreased the expression of Nogo-A, p75NTR, and ROCKII both in and around the LEp. Conclusion. CIG improved the locomotor impairment, decreased tissue damage, and downregulated the myelin-associated inhibition signaling pathway in SCI rats. The results suggest that CIG may be beneficial for SCI therapy.

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