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 Berberine protects 6-hydroxydopamine-induced human dopaminergic neuronal cell death through the induction of heme oxygenase-1

2013 ◽  
Vol 35 (2) ◽  
pp. 151-157 ◽  
Author(s):  
Jinbum Bae ◽  
Danbi Lee ◽  
Yun Kyu Kim ◽  
Minchan Gil ◽  
Joo-Yong Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Heme Oxygenase ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Heme Oxygenase 1 ◽  
Dopaminergic Neuronal Cell ◽  
6 Hydroxydopamine

scholarly journals Betulin Protects HT-22 Hippocampal Cells against ER Stress through Induction of Heme Oxygenase-1 and Inhibition of ROS Production

2019 ◽  
Vol 14 (12) ◽  
pp. 1934578X1989668 ◽  
Author(s):  
Phil Jun Lee ◽  
Hye-Jin Park ◽  
Hee Min Yoo ◽  
Namki Cho
Keyword(s):  
Cell Death ◽  
Neurodegenerative Diseases ◽  
Er Stress ◽  
Heme Oxygenase ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ros Generation ◽  
Heme Oxygenase 1 ◽  
Ros Scavenging ◽  
Neuroprotective Effects

A key pathologic event in neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, is endoplasmic reticulum (ER) stress-induced neuronal cell death. ER stress-induced generation of reactive oxygen species (ROS) has been implicated in neurological disease processes. Betulin is one of the major triterpenoids found in Betula platyphylla that possesses several biological properties, including cytoprotective and antioxidative effects. Therefore, we investigated whether betulin could prevent ER stress-induced neurotoxicity in HT-22 hippocampal neuronal cells. We observed that betulin reduced the thapsigargin (TG, an ER stress inducer)-induced apoptosis of HT-22 cells. Moreover, the cytoprotective effects of betulin were comparable to those of tauroursodeoxycholic acid, a potent ER stress-reducing agent. In our study, we confirmed that the ER stress-induced accumulation of ROS plays an important role in HT-22 cell death. Betulin also displayed cytoprotective effects in TG-injured HT-22 cells by reducing ROS generation; these results were comparable to those for N-acetyl-L-cysteine, a known ROS inhibitor. In addition, SnPP, a heme oxygenase-1 (HO-1) inhibitor significantly blocked the cytoprotective effects and ROS scavenging activity of betulin. Based on these results, we believe that betulin-mediated induction of HO-1 may contribute to the neuroprotective effects against ER stress in HT-22 hippocampal cells. We also found that betulin significantly inhibited the TG-induced expression of CHOP and caspase-12. These results demonstrated that betulin could serve as a potential therapeutic agent against ER stress-induced neurodegenerative diseases.

scholarly journals Desipramine Protects Neuronal Cell Death and Induces Heme Oxygenase-1 Expression in Mes23.5 Dopaminergic Neurons

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e50138 ◽  
Author(s):  
Hsiao-Yun Lin ◽  
Wei-Lan Yeh ◽  
Bor-Ren Huang ◽  
Chingju Lin ◽  
Chih-Ho Lai ◽  
...  
Keyword(s):  
Cell Death ◽  
Heme Oxygenase ◽  
Dopaminergic Neurons ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Heme Oxygenase 1

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

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 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.

Sign in / Sign up

Export Citation Format

Share Document