Pulsed electromagnetic field and relief of hypoxia‐induced neuronal cell death: The signaling pathway

2019 ◽  
Vol 234 (9) ◽  
pp. 15089-15097 ◽  
Author(s):  
Stefania Gessi ◽  
Stefania Merighi ◽  
Serena Bencivenni ◽  
Enrica Battistello ◽  
Fabrizio Vincenzi ◽  
...  
Keyword(s):  
Cell Death ◽  
Electromagnetic Field ◽  
Signaling Pathway ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Pulsed Electromagnetic Field ◽  
Pulsed Electromagnetic

scholarly journals Neuroprotection after Hemorrhagic Stroke Depends on Cerebral Heme Oxygenase-1

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 496 ◽  
Author(s):  
Sandra Kaiser ◽  
Sibylle Frase ◽  
Lisa Selzner ◽  
Judith-Lisa Lieberum ◽  
Jakob Wollborn ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebrospinal Fluid ◽  
Functional Outcome ◽  
Signaling Pathway ◽  
Heme Oxygenase ◽  
Hemorrhagic Stroke ◽  
Mrna Level ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Heme Oxygenase 1

(1) Background: A detailed understanding of the pathophysiology of hemorrhagic stroke is still missing. We hypothesized that expression of heme oxygenase-1 (HO-1) in microglia functions as a protective signaling pathway. (2) Methods: Hippocampal HT22 neuronal cells were exposed to heme-containing blood components and cell death was determined. We evaluated HO-1-induction and cytokine release by wildtype compared to tissue-specific HO-1-deficient (LyzM-Cre.Hmox1 fl/fl) primary microglia (PMG). In a study involving 46 patients with subarachnoid hemorrhage (SAH), relative HO-1 mRNA level in the cerebrospinal fluid were correlated with hematoma size and functional outcome. (3) Results: Neuronal cell death was induced by exposure to whole blood and hemoglobin. HO-1 was induced in microglia following blood exposure. Neuronal cells were protected from cell death by microglia cell medium conditioned with blood. This was associated with a HO-1-dependent increase in monocyte chemotactic protein-1 (MCP-1) production. HO-1 mRNA level in the cerebrospinal fluid of SAH-patients correlated positively with hematoma size. High HO-1 mRNA level in relation to hematoma size were associated with improved functional outcome at hospital discharge. (4) Conclusions: Microglial HO-1 induction with endogenous CO production functions as a crucial signaling pathway in blood-induced inflammation, determining microglial MCP-1 production and the extent of neuronal cell death. These results give further insight into the pathophysiology of neuronal damage after SAH and the function of HO-1 in humans.

scholarly journals Regulation of Neuronal Cell Death by c-Abl-Hippo/MST2 Signaling Pathway

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e36562 ◽  
Author(s):  
Weizhe Liu ◽  
Junbing Wu ◽  
Lei Xiao ◽  
Yujie Bai ◽  
Aiqin Qu ◽  
...  
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals The c-Abl-MST1 Signaling Pathway Mediates Oxidative Stress-Induced Neuronal Cell Death

2011 ◽  
Vol 31 (26) ◽  
pp. 9611-9619 ◽  
Author(s):  
L. Xiao ◽  
D. Chen ◽  
P. Hu ◽  
J. Wu ◽  
W. Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Signaling Pathway ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Deregulation of the Egfr/Ras Signaling Pathway Induces Age-related Brain Degeneration in the Drosophila Mutantvap

2003 ◽  
Vol 14 (1) ◽  
pp. 241-250 ◽  
Author(s):  
José A. Botella ◽  
Doris Kretzschmar ◽  
Claudia Kiermayer ◽  
Pascale Feldmann ◽  
David A. Hughes ◽  
...  
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Egf Receptor ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ras Signaling ◽  
Age Related ◽  
Receptor Signaling Pathway ◽  
Brain Degeneration

Ras signaling has been shown to play an important role in promoting cell survival in many different tissues. Here we show that upregulation of Ras activity in adult Drosophila neurons induces neuronal cell death, as evident from the phenotype of vacuolar peduncle (vap) mutants defective in theDrosophila RasGAP gene, which encodes a Ras GTPase-activating protein. These mutants show age-related brain degeneration that is dependent on activation of the EGF receptor signaling pathway in adult neurons, leading to autophagic cell death (cell death type 2). These results provide the first evidence for a requirement of Egf receptor activity in differentiated adultDrosophila neurons and show that a delicate balance of Ras activity is essential for the survival of adult neurons.

scholarly journals Effect of Pulsed Electromagnetic Field on Bone Formation and Lipid Metabolism of Glucocorticoid-Induced Osteoporosis Rats through Canonical Wnt Signaling Pathway

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Yuan Jiang ◽  
Hui Gou ◽  
Sanrong Wang ◽  
Jiang Zhu ◽  
Si Tian ◽  
...  
Keyword(s):  
Electromagnetic Field ◽  
Lipid Metabolism ◽  
Bone Formation ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Pulsed Electromagnetic Field ◽  
Canonical Wnt Signaling ◽  
Pulsed Electromagnetic ◽  
Canonical Wnt

Pulsed electromagnetic field (PEMF) has been suggested as a promising method alternative to drug-based therapies for treating osteoporosis (OP), but the role of PEMF in GIOP animal models still remains unknown. This study was performed to investigate the effect of PEMF on bone formation and lipid metabolism and further explored the several important components and targets of canonical Wnt signaling pathway in GIOP rats. After 12 weeks of intervention, bone mineral density (BMD) level of the whole body increased significantly, serum lipid levels decreased significantly, and trabeculae were thicker in GIOP rats of PEMF group. PEMF stimulation upregulated the mRNA and protein expression of Wnt10b, LRP5,β-catenin, OPG, and Runx2 and downregulated Axin2, PPAR-γ, C/EBPα, FABP4, and Dkk-1. The results of this study suggested that PEMF stimulation can prevent bone loss and improve lipid metabolism disorders in GIOP rats. Canonical Wnt signaling pathway plays an important role in bone formation and lipid metabolism during PEMF stimulation.

Involvement of SAPK/JNK Signaling Pathway in Copper Enhanced Zinc-Induced Neuronal Cell Death

2019 ◽  
Vol 169 (1) ◽  
pp. 293-302 ◽  
Author(s):  
Ken-Ichiro Tanaka ◽  
Mikako Shimoda ◽  
Misato Kasai ◽  
Mayumi Ikeda ◽  
Yu Ishima ◽  
...  
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway
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