scholarly journals Regulation of Cytokine-Induced Neuron Death by Ovarian Hormones: Involvement of Antiapoptotic Protein Expression and c-JUN N-Terminal Kinase-Mediated Proapoptotic Signaling

Endocrinology ◽  
2004 ◽  
Vol 145 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Carol Lee Koski ◽  
Sorana Hila ◽  
Gloria E. Hoffman
Keyword(s):  
Protein Expression ◽  
Ovarian Hormones ◽  
Neuron Death ◽  
Antiapoptotic Protein ◽  
Induced Neuron

scholarly journals The Transient Receptor Potential Melastatin 7 (TRPM7) Inhibitors Suppress Seizure-Induced Neuron Death by Inhibiting Zinc Neurotoxicity

2020 ◽  
Vol 21 (21) ◽  
pp. 7897
Author(s):  
Jeong Hyun Jeong ◽  
Song Hee Lee ◽  
A Ra Kho ◽  
Dae Ki Hong ◽  
Dong Hyeon Kang ◽  
...  
Keyword(s):  
Transient Receptor Potential ◽  
Therapeutic Potential ◽  
Divalent Cations ◽  
Neurological Diseases ◽  
Receptor Potential ◽  
Neuron Death ◽  
Intracellular Zinc ◽  
Transient Receptor Potential Melastatin ◽  
Transient Receptor ◽  
Induced Neuron

Transient receptor potential melastatin 7 (TRPM7) is an ion channel that mediates monovalent cations out of cells, as well as the entry of divalent cations, such as zinc, magnesium, and calcium, into the cell. It has been reported that inhibitors of TRPM7 are neuroprotective in various neurological diseases. Previous studies in our lab suggested that seizure-induced neuronal death may be caused by the excessive release of vesicular zinc and the subsequent accumulation of zinc in the neurons. However, no studies have evaluated the effects of carvacrol and 2-aminoethoxydiphenyl borate (2-APB), both inhibitors of TRPM7, on the accumulation of intracellular zinc in dying neurons following seizure. Here, we investigated the therapeutic efficacy of carvacrol and 2-APB against pilocarpine-induced seizure. Carvacrol (50 mg/kg) was injected once per day for 3 or 7 days after seizure. 2-APB (2 mg/kg) was also injected once per day for 3 days after seizure. We found that inhibitors of TRPM7 reduced seizure-induced TRPM7 overexpression, intracellular zinc accumulation, and reactive oxygen species production. Moreover, there was a suppression of oxidative stress, glial activation, and the blood–brain barrier breakdown. In addition, inhibitors of TRPM7 remarkably decreased apoptotic neuron death following seizure. Taken together, the present study demonstrates that TRPM7-mediated zinc translocation is involved in neuron death after seizure. The present study suggests that inhibitors of TRPM7 may have high therapeutic potential to reduce seizure-induced neuron death.

scholarly journals The regulation of p53 up-regulated modulator of apoptosis by JNK/c-Jun pathway in β-amyloid-induced neuron death

2015 ◽  
Vol 134 (6) ◽  
pp. 1091-1103 ◽  
Author(s):  
Rumana Akhter ◽  
Priyankar Sanphui ◽  
Hrishita Das ◽  
Pampa Saha ◽  
Subhas Chandra Biswas
Keyword(s):  
Neuron Death ◽  
Β Amyloid ◽  
Induced Neuron

Glutamate-induced neuron death requires mitochondrial calcium uptake

10.1038/1577 ◽  
1998 ◽  
Vol 1 (5) ◽  
pp. 366-373 ◽  
Author(s):  
Amy K. Stout ◽  
Heather M. Raphael ◽  
Beatriz I. Kanterewicz ◽  
Eric Klann ◽  
Ian J. Reynolds
Keyword(s):  
Calcium Uptake ◽  
Mitochondrial Calcium ◽  
Neuron Death ◽  
Induced Neuron ◽  
Mitochondrial Calcium Uptake

P3-299 TNF death receptor signaling cascade is required for amyloid-β protein induced neuron death

2004 ◽  
Vol 25 ◽  
pp. S440
Author(s):  
Yong Shen ◽  
Rena Li ◽  
Libang Yang ◽  
Kristina Lindholm ◽  
Yoshihiro Konishi ◽  
...  
Keyword(s):  
Death Receptor ◽  
Amyloid Β ◽  
Signaling Cascade ◽  
Amyloid Β Protein ◽  
Receptor Signaling ◽  
Neuron Death ◽  
Β Protein ◽  
Death Receptor Signaling ◽  
Induced Neuron

Abstract WMP70: HIF-1alpha Sumoylation Provides Neuroprotection in Ischemic Stroke

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Jingqi Yan ◽  
Honglian Shi
Keyword(s):  
Therapeutic Target ◽  
Hypoxia Inducible Factor ◽  
Artery Occlusion ◽  
Neuron Death ◽  
Ischemic Brain ◽  
Hypoxia Inducible Factor 1 ◽  
Induced Neuron ◽  
Cerebral Artery Occlusion ◽  
First Time

Hypoxia-inducible factor 1 (HIF-1) is a transcriptional factor that regulates the cellular adaptive response to hypoxia and has been suggested as a potent therapeutic target in stroke. To find new post-transpational modification pathways of HIF-1 in ischemic brain, we determined SUMOylation of HIF-1α protein in ischemic brain of a rat middle cerebral artery occlusion (MCAO) stroke model. The results demonstrated that SUMOylation of HIF-1α by SUMO1 was increased in the ischemic brain. Immunostaining images showed that HIF-1α co-localized with SUMO1 in the neuron nucleus of the ischemic brain. Inhibition of HIF-1α SUMOylation by Ubc9 siRNA reduced HIF-1α protein level in primary neurons during hypoxia. Furthermore, ischemia-induced neuron death was increased by the Ubc9 siRNA. The results, for the first time, demonstrate that HIF-1α is directly SUMOylated in the ischemic brain. HIF-1α SUMOylation is important for HIF-1α stability and neuron survival during ischemia. These results complement the knowledge about HIF-1 regulation in ischemic brain and shed new light on the role of HIF-1 as a stroke therapeutic target.

CCL3L1 prevents gp120-induced neuron death via the CREB cell signaling pathway

2009 ◽  
Vol 1257 ◽  
pp. 75-88 ◽  
Author(s):  
Huang Chun ◽  
Wu Hao ◽  
Zhang Honghai ◽  
Li Ning ◽  
Wu Yasong ◽  
...  
Keyword(s):  
Cell Signaling ◽  
Signaling Pathway ◽  
Neuron Death ◽  
Cell Signaling Pathway ◽  
Induced Neuron
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