scholarly journals Zinc Oxide Nanoparticles Induce Ferroptotic Neuronal Cell Death in vitro and in vivo

2020 ◽  
Vol Volume 15 ◽  
pp. 5299-5315
Author(s):  
Xia Qin ◽  
Qianghu Tang ◽  
Xuejun Jiang ◽  
Jun Zhang ◽  
Bin Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Oxide Nanoparticles

scholarly journals Fenugreek-mediated synthesis of zinc oxide nanoparticles and evaluation of its in vitro and in vivo antitumor potency

2021 ◽  
Vol 8 (8) ◽  
pp. 4483-4496
Author(s):  
Aliaa M. Radwan ◽  
Eman F. Aboelfetoh ◽  
Tetsunari Kimura ◽  
Tarek M. Mohamed ◽  
Mai M. El-Keiy
Keyword(s):  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Oxide Nanoparticles

Selective Release of Calpain Produced αII-Spectrin (α-Fodrin) Breakdown Products by Acute Neuronal Cell Death

2002 ◽  
Vol 383 (5) ◽  
pp. 785-791 ◽  
Author(s):  
Satavisha Dutta ◽  
Yuk Chun Chiu ◽  
Albert W. Probert ◽  
Kevin K.W. Wang
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Neuronal Injury ◽  
Nmda Receptor Antagonist ◽  
Breakdown Product ◽  
Calpain Inhibitor ◽  
Neural Cells

Abstract Activation of calpain results in the breakdown of α II spectrin (αfodrin), a neuronal cytoskeleton protein, which has previously been detected in various in vitro and in vivo neuronal injury models. In this study, a 150 kDa spectrin breakdown product (SBDP150) was found to be released into the cellconditioned media from SHSY5Y cells treated with the calcium channel opener maitotoxin (MTX). SBDP150 release can be readily quantified on immunoblot using an SBDP150- specific polyclonal antibody. Increase of SBDP150 also correlated with cell death in a timedependent manner. MDL28170, a selective calpain inhibitor, was the only protease inhibitor tested that significantly reduced MTXinduced SBDP150 release. The cellconditioned media of cerebellar granule neurons challenged with excitotoxins (NMDA and kainate) also exhibited a significant increase of SBDP150 that was attenuated by pretreatment with an NMDA receptor antagonist, R()-3-(2-carbopiperazine-4-yl)propyl-1- phosphonic acid (CPP), and MDL28170. In addition, hypoxic/hypoglycemic challenge of cerebrocortical cultures also resulted in SBDP150 liberation into the media. These results support the theory that an antibody based detection of SBDP150 in the cellconditioned media can be utilized to quantify injury to neural cells. Furthermore, SBDP150 may potentially be used as a surrogate biomarker for acute neuronal injury in clinical settings.

scholarly journals Cylindromatosis mediates neuronal cell death in vitro and in vivo

2018 ◽  
Vol 25 (8) ◽  
pp. 1394-1407 ◽  
Author(s):  
Goutham K. Ganjam ◽  
Nicole Angela Terpolilli ◽  
Sebastian Diemert ◽  
Ina Eisenbach ◽  
Lena Hoffmann ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Degradation of mutant huntingtin via the ubiquitin/proteasome system is modulated by FE65

2012 ◽  
Vol 443 (3) ◽  
pp. 681-689 ◽  
Author(s):  
Wan Ning Vanessa Chow ◽  
Hon Wing Luk ◽  
Ho Yin Edwin Chan ◽  
Kwok-Fai Lau
Keyword(s):  
Cell Death ◽  
Degradation Mechanism ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Adaptor Protein ◽  
Ubiquitin Proteasome System ◽  
Exon 1 ◽  
Ubiquitin Proteasome

An unstable expansion of the polyglutamine repeat within exon 1 of the protein Htt (huntingtin) causes HD (Huntington's disease). Mounting evidence shows that accumulation of N-terminal mutant Htt fragments is the source of disruption of normal cellular processes which ultimately leads to neuronal cell death. Understanding the degradation mechanism of mutant Htt and improving its clearance has emerged as a new direction in developing therapeutic approaches to treat HD. In the present study we show that the brain-enriched adaptor protein FE65 is a novel interacting partner of Htt. The binding is mediated through WW–polyproline interaction and is dependent on the length of the polyglutamine tract. Interestingly, a reduction in mutant Htt protein level was observed in FE65-knockdown cells, and the process requires the UPS (ubiquitin/proteasome system). Moreover, the ubiquitination level of mutant Htt was found to be enhanced when FE65 is knocked down. Immunofluroescence staining revealed that FE65 associates with mutant Htt aggregates. Additionally, we demonstrated that overexpression of FE65 increases mutant Htt-induced cell death both in vitro and in vivo. These results suggest that FE65 facilitates the accumulation of mutant Htt in cells by preventing its degradation via the UPS, and thereby enhances the toxicity of mutant Htt.

Effects of PACAP on in vitro and in vivo neuronal cell death, platelet aggregation, and production of reactive oxygen radicals

2004 ◽  
Vol 123 (1-3) ◽  
pp. 51-59 ◽  
Author(s):  
Dóra Reglödi ◽  
Zsolt Fábián ◽  
Andrea Tamás ◽  
Andrea Lubics ◽  
József Szeberényi ◽  
...  
Keyword(s):  
Cell Death ◽  
Platelet Aggregation ◽  
Oxygen Radicals ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Reactive Oxygen

scholarly journals Effects of Zinc Oxide Nanoparticles Synthesized Using Aspergillus niger on Carbapenem-Resistant Klebsiella pneumonia In Vitro and In Vivo

2021 ◽  
Vol 11 ◽  
Author(s):  
Elsayim Rasha ◽  
Manal M. Alkhulaifi ◽  
Monerah AlOthman ◽  
Ibrahim Khalid ◽  
Elnagar Doaa ◽  
...  
Keyword(s):  
Zinc Oxide ◽  
Aspergillus Niger ◽  
Zinc Oxide Nanoparticles ◽  
Diffusion Method ◽  
Oxide Nanoparticles ◽  
Zno Nps ◽  
X Ray ◽  
Carbapenem Resistant

Currently, the mortality rate in Saudi Arabia’s ICUs is increasing due to the spread of Klebsiella pneumoniae carbapenemase (KPC)-producing bacteria. This study was carried out to evaluate the ability of biologically synthesized zinc oxide nanoparticles (ZnO-NPs) using Aspergillus niger to overcome carbapenem-resistant K. pneumoniae (KPC) in vitro and in vivo. ZnO-NPs were synthesized via a biological method and characterized using UV–Vis spectroscopy, Zetasizer and zeta potential analyses, x-ray diffraction spectroscopy, Fourier transform infrared spectroscopy, scanning electron microscopy (SEM), and energy-dispersive x-ray spectroscopy (EDX). In vitro sensitivity of KPC to ZnO-NPs was identified using the well diffusion method. The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) were determined by a macro-dilution method. The morphological alteration of KPC cells after ZnO-NPs treatment was observed by SEM. The in vivo susceptibility of KPC cells to ZnO-NPs ointment was evaluated using wound healing in experimental rats. The chemical characterization findings showed the formation, stability, shape, and size of the synthesized nanoparticles. The MIC and MBC were 0.7 and 1.8 mg/ml, respectively. The in vivo results displayed reduced inflammation and wound re-epithelialization of KPC-infected rats. These findings demonstrated that ZnO-NPs have great potential to be developed as antibacterial agents.

No effect of apolipoprotein E on neuronal cell death due to excitotoxic and apoptotic agents in vitro and neonatal hypoxic ischaemia in vivo

2000 ◽  
Vol 12 (7) ◽  
pp. 2235-2242 ◽  
Author(s):  
Corinne L. Lendon ◽  
Byung Hee Han ◽  
Kayvon Salimi ◽  
Anne M. Fagan ◽  
Maria I. Behrens ◽  
...  
Keyword(s):  
Cell Death ◽  
Apolipoprotein E ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Alteration of gene expression by zinc oxide nanoparticles or zinc sulfate in vivo and comparison with in vitro data: A harmonious case

2016 ◽  
Vol 86 (3) ◽  
pp. 850-861.e1 ◽  
Author(s):  
Wei-Dong Zhang ◽  
Yong Zhao ◽  
Hong-Fu Zhang ◽  
Shu-Kun Wang ◽  
Zhi-Hui Hao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Zinc Oxide ◽  
Zinc Oxide Nanoparticles ◽  
Zinc Sulfate ◽  
Oxide Nanoparticles ◽  
Vitro Data ◽  
In Vitro Data

Influence of corticotrophin releasing factor on neuronal cell death in vitro and in vivo

2000 ◽  
Vol 881 (2) ◽  
pp. 139-143 ◽  
Author(s):  
Mark W. Craighead ◽  
Herve Boutin ◽  
Kelly M.L. Middlehurst ◽  
Stuart M. Allan ◽  
Nigel Brooks ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Corticotrophin Releasing Factor

scholarly journals Prokineticin-2 prevents neuronal cell deaths in a model of traumatic brain injury

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Zhongyuan Bao ◽  
Yinlong Liu ◽  
Binglin Chen ◽  
Zong Miao ◽  
Yiming Tu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Cell Death ◽  
Brain Injury ◽  
Neuronal Degeneration ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Prokineticin 2

AbstractProkineticin-2 (Prok2) is an important secreted protein likely involved in the pathogenesis of several acute and chronic neurological diseases through currently unidentified regulatory mechanisms. The initial mechanical injury of neurons by traumatic brain injury triggers multiple secondary responses including various cell death programs. One of these is ferroptosis, which is associated with dysregulation of iron and thiols and culminates in fatal lipid peroxidation. Here, we explore the regulatory role of Prok2 in neuronal ferroptosis in vitro and in vivo. We show that Prok2 prevents neuronal cell death by suppressing the biosynthesis of lipid peroxidation substrates, arachidonic acid-phospholipids, via accelerated F-box only protein 10 (Fbxo10)-driven ubiquitination, degradation of long-chain-fatty-acid-CoA ligase 4 (Acsl4), and inhibition of lipid peroxidation. Mice injected with adeno-associated virus-Prok2 before controlled cortical impact injury show reduced neuronal degeneration and improved motor and cognitive functions, which could be inhibited by Fbxo10 knockdown. Our study shows that Prok2 mediates neuronal cell deaths in traumatic brain injury via ferroptosis.

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