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 ◽  
...  
Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 496 ◽  
Author(s):  
Sandra Kaiser ◽  
Sibylle Frase ◽  
Lisa Selzner ◽  
Judith-Lisa Lieberum ◽  
Jakob Wollborn ◽  
...  

(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.


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

2019 ◽  
Vol 234 (9) ◽  
pp. 15089-15097 ◽  
Author(s):  
Stefania Gessi ◽  
Stefania Merighi ◽  
Serena Bencivenni ◽  
Enrica Battistello ◽  
Fabrizio Vincenzi ◽  
...  

2019 ◽  
Vol 16 (8) ◽  
Author(s):  
Yingxiang Liu ◽  
Ziting Ren ◽  
Xiang Li ◽  
Jing Zhong ◽  
Yun Bi ◽  
...  

2011 ◽  
Vol 31 (26) ◽  
pp. 9611-9619 ◽  
Author(s):  
L. Xiao ◽  
D. Chen ◽  
P. Hu ◽  
J. Wu ◽  
W. Liu ◽  
...  

2003 ◽  
Vol 14 (1) ◽  
pp. 241-250 ◽  
Author(s):  
José A. Botella ◽  
Doris Kretzschmar ◽  
Claudia Kiermayer ◽  
Pascale Feldmann ◽  
David A. Hughes ◽  
...  

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.


BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Zehui Li ◽  
Nneka E. Mbah ◽  
Jean H. Overmeyer ◽  
Jeffrey G. Sarver ◽  
Sage George ◽  
...  

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