Eriodictyol protects against H2O2-induced neuron-like PC12 cell death through activation of Nrf2/ARE signaling pathway

2012 ◽  
Vol 61 (2) ◽  
pp. 251-257 ◽  
Author(s):  
Haiyan Lou ◽  
Xu Jing ◽  
Dongmei Ren ◽  
Xinbing Wei ◽  
Xiumei Zhang
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Pc12 Cell ◽  
Induced Neuron

bFGF expression mediated by a hypoxia-regulated adenoviral vector protects PC12 cell death induced by serum deprivation

2009 ◽  
Vol 390 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Hou-Wen Hu ◽  
Xiao-Kun Li ◽  
Rong-Yuan Zheng ◽  
Jian Xiao ◽  
Jin-Qi Zeng ◽  
...  
Keyword(s):  
Cell Death ◽  
Pc12 Cell ◽  
Adenoviral Vector ◽  
Serum Deprivation

Mechanisms of Manganese-Induced Rat Pheochromocytoma (PC12) Cell Death and Cell Differentiation

2002 ◽  
Vol 23 (2) ◽  
pp. 147-157 ◽  
Author(s):  
Jerome A. Roth ◽  
Craig Horbinski ◽  
Dennis Higgins ◽  
Pamela Lein ◽  
Michael D. Garrick
Keyword(s):  
Cell Death ◽  
Cell Differentiation ◽  
Pc12 Cell ◽  
Pheochromocytoma Pc12

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 Internucleosomal DNA cleavage and neuronal cell survival/death

1993 ◽  
Vol 122 (3) ◽  
pp. 523-532 ◽  
Author(s):  
A Batistatou ◽  
LA Greene
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Dna Fragmentation ◽  
Cell Cultures ◽  
Pc12 Cell ◽  
Dna Cleavage ◽  
Sympathetic Neurons ◽  
Term Survival ◽  
Serum Withdrawal

Serum-free PC12 cell cultures have been used to study the mechanisms of neuronal death after neurotrophic factor deprivation. We previously reported that PC12 cells undergo "apoptotic" internucleosomal DNA cleavage after withdrawal of trophic support. Here, we have used a sensitive method to detect PC12 cell DNA fragmentation within three hrs of serum removal and have exploited this assay to examine several aspects regarding the mechanisms of neuronal survival/death. Major advantages of this assay are that it permits acute experiments to be performed well before other manifest signs of cell death and under conditions that cannot be applied chronically. We find that this apopotic DNA fragmentation is distinct from the random DNA degradation that occurs during necrotic death. Major observations include the following: (a) There is a good correlation between the ability of trophic substances to promote PC12 cell survival and to inhibit early DNA fragmentation. (b) Phorbol ester, an activator of PKC, acutely suppresses DNA fragmentation, but does not promote long-term survival or inhibition of endonuclease activity when applied chronically due to its downregulation of PKC. (c) Cells undergoing apoptosis within 3 h of serum withdrawal have a "commitment point" of only 1.0-1.5 h beyond which they can no longer be rescued by NGF. (d) Aurin, a non-carboxylic analog of the endonuclease inhibitor ATA, also inhibits DNA fragmentation and promotes short-term survival of PC12 cells. (e) Macromolecular synthesis is not required for DNA fragmentation or for NGF to prevent this event. (f) Extracellular Ca2+ is not required for internucleosomal DNA cleavage caused by serum withdrawal or for suppression of this by NGF. (g) DNA fragmentation can also be detected in cultures of rat sympathetic neurons as early as 10 h after removal of NGF. As in PC12 cell cultures, this precedes morphological signs of cell death.

PCSK9 Promotes oxLDL-Induced PC12 Cell Apoptosis Through the Bcl-2/Bax-Caspase 9/3 Signaling Pathway

2017 ◽  
Vol 57 (3) ◽  
pp. 723-734 ◽  
Author(s):  
Lu-Shan Liu ◽  
Xue-Qin Bai ◽  
Ya Gao ◽  
Qi Wu ◽  
Zhong Ren ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pc12 Cell ◽  
Cell Apoptosis ◽  
Caspase 9

scholarly journals Nitrate Efflux Is an Essential Component of the Cryptogein Signaling Pathway Leading to Defense Responses and Hypersensitive Cell Death in Tobacco

2002 ◽  
Vol 14 (8) ◽  
pp. 1937-1951 ◽  
Author(s):  
David Wendehenne ◽  
Olivier Lamotte ◽  
Jean-Marie Frachisse ◽  
Hélène Barbier-Brygoo ◽  
Alain Pugin
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Defense Responses ◽  
Hypersensitive Cell Death ◽  
Essential Component

scholarly journals Sequence Analysis and Homology Modeling of NF2 Protein

2019 ◽  
pp. 373-377
Author(s):  
Vinod P. Sinoorkar ◽  
Pratiksha S. Thakurdas
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Actin Binding ◽  
Hippo Signaling ◽  
Β Cell ◽  
Neurofibromatosis 2 ◽  
Pancreatic Cell ◽  
Hippo Signaling Pathway ◽  
Molecular Features ◽  
Chronic Hyperglycemia

Diabetes is diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion, insulin action, or both. In India more than 62 million individuals currently diagnosed with the diabetes. Diabetes is resulting from insulin deficiency or pancreatic cells become insulin resistant. Pancreatic cell (β-cell) death by apoptosis is one of main reason which results in diabetic condition in patients. Neurofibromatosis 2 is involved is β-cell death. Neurofibromatosis 2 (NF2/Merlin) is a tumor suppressor protein, which belongs to the ezrin–radixin–moesin family of actin-binding proteins and regulates the Hippo signaling pathway in mammals and also involved in the regulation of cell proliferation and apoptosis. Merlin regulates the Hippo signaling pathway by controlling the Hippo kinases cassettes MST1/2 and LATS1/2. Therefore, targeting β-cell apoptosis and dysfunction can be a therapeutic approach for the treatment of diabetes. Hence our present investigation focus mainly to understand the detailed molecular features of NF2 by its protein sequence annotation by implementing tools and techniques of Bioinformatics.

scholarly journals ZBP1 induces inflammatory signaling via RIPK3 and promotes SARS-CoV-2-induced cytokine expression

2021 ◽  
Author(s):  
Ruoshi Peng ◽  
Xuan Wang-Kan ◽  
Manja Idorn ◽  
Felix Y Zhou ◽  
Susana L Orozco ◽  
...  
Keyword(s):  
Cell Death ◽  
Signaling Pathway ◽  
Kinase Activity ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Innate Immune Responses ◽  
Inflammatory Signaling ◽  
Antiviral Responses ◽  
Nucleic Acid Sensor ◽  
Activity Dependent

AbstractCOVID-19 caused by the SARS-CoV-2 virus remains a threat to global health. The disease severity is mediated by cell death and inflammation, which regulate both the antiviral and the pathological innate immune responses. ZBP1, an interferon-induced cytosolic nucleic acid sensor, facilitates antiviral responses via RIPK3. Although ZBP1-mediated cell death is widely described, whether and how it promotes inflammatory signaling is unclear. Here, we report a ZBP1-induced inflammatory signaling pathway that depends on ubiquitination and RIPK3’s scaffolding ability independently of cell death. In human cells, ZBP1 associates with RIPK1 and RIPK3 as well as ubiquitin ligases cIAP1 and LUBAC. RIPK1 and ZBP1 are ubiquitinated to promote TAK1- and IKK-mediated inflammatory signaling. Additionally, RIPK1 recruits the p43/41-caspase-8-p43-FLIP heterodimer to suppress RIPK3 kinase activity, which otherwise promotes inflammatory signaling in a kinase activity-dependent manner. Lastly, we show that ZBP1 contributes to SARS-CoV-2-induced cytokine production. Taken together, we describe a ZBP1-RIPK1-RIPK3-mediated inflammatory signaling pathway relayed by the scaffolding role of RIPKs and regulated by caspase-8. Our results suggest the ZBP1 pathway contributes to inflammation in response to SARS-CoV-2 infection.

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