scholarly journals Synergy and antagonism of macroautophagy and chaperone-mediated autophagy in a cell model of pathological tau aggregation

Autophagy ◽  
2010 ◽  
Vol 6 (1) ◽  
pp. 182-183 ◽  
Author(s):  
Yipeng Wang ◽  
Marta Martinez-Vicente ◽  
Ulrike Krüger ◽  
Susmita Kaushik ◽  
Esther Wong ◽  
...  
Keyword(s):  
Cell Model ◽  
A Cell ◽  
Tau Aggregation ◽  
Chaperone Mediated Autophagy

[P4-102]: CHARACTERISATION OF MOLECULAR MECHANISMS THAT ARE TRIGGERED AND CONTRIBUTE TO TAU PATHOLOGY IN A CELL MODEL OF TAU AGGREGATION

2017 ◽  
Vol 13 (7S_Part_27) ◽  
pp. P1297-P1297
Author(s):  
Emma Mead ◽  
Elena Ficulle ◽  
Charlotte Dunbar ◽  
Sarah Eversden ◽  
Michael J. O'Neill ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cell Model ◽  
Tau Pathology ◽  
A Cell ◽  
Tau Aggregation

Proteolytic processing of tau

2010 ◽  
Vol 38 (4) ◽  
pp. 955-961 ◽  
Author(s):  
Yipeng Wang ◽  
Sarika Garg ◽  
Eva-Maria Mandelkow ◽  
Eckhard Mandelkow
Keyword(s):  
Neurodegenerative Diseases ◽  
Therapeutic Approach ◽  
Cell Model ◽  
Proteolytic Processing ◽  
The Other ◽  
Promising Therapeutic Approach ◽  
A Cell ◽  
Ad Alzheimer’S Disease ◽  
Tau Aggregation ◽  
Tau Cleavage

Tau aggregation is a hallmark of several neurodegenerative diseases, including AD (Alzheimer's disease), although the mechanism underlying tau aggregation remains unclear. Recent studies show that the proteolysis of tau plays an important role in both tau aggregation and neurodegeneration. On one hand, truncation of tau may generate amyloidogenic tau fragments that initiate the aggregation of tau, which in turn can cause toxicity. On the other hand, truncation of tau may result in tau fragments which induce neurodegeneration through unknown mechanisms, independently of tau aggregation. Blocking the truncation of tau thus may represent a promising therapeutic approach for AD or other tauopathies. In the present paper, we summarize our data on tau cleavage in a cell model of tauopathy and major results on tau cleavage reported in the literature.

scholarly journals Visualization of Tau–Tubulin Interaction in a Living Cell Using Bifluorescence Complementation Technique

2018 ◽  
Vol 19 (10) ◽  
pp. 2978 ◽  
Author(s):  
Seulgi Shin ◽  
Sungsu Lim ◽  
Hyeanjeong Jeong ◽  
Li Kwan ◽  
Yun Kim
Keyword(s):  
Neurodegenerative Disorders ◽  
Living Cell ◽  
Neuronal Degeneration ◽  
Cell Model ◽  
Chemical Stimulation ◽  
Aggregation Process ◽  
Phosphorylated Tau ◽  
Tau Pathology ◽  
A Cell ◽  
Tau Aggregation

Tau is a neuron-specific microtubule-binding protein that stabilizes microtubules. It is generally thought that highly phosphorylated tau dissociates from microtubules and becomes insoluble aggregates, leading to neuronal degeneration. Due to the implication of tau aggregation in neurodegenerative disorders, including Alzheimer’s disease, great efforts have been made to identify the tau aggregation process. However, tau interaction with tubulin during the aggregation process remains largely unknown. To scrutinize the tau-tubulin interaction, we generated a cell model that enables visualization of the tau-tubulin interaction in a living cell using the Bifluorescence Complementation (BiFC) Technique. Upon diverse chemical stimulation that induced tau pathology, tau-tubulin BiFC cells showed significantly increased levels of BiFC fluorescence, indicating that tau aggregates together with tubulin. Our results suggest that tubulin should be considered as a key component in the tau aggregation process.

INVERSE UNCERTAINTY QUANTIFICATION OF A CELL MODEL USING A GAUSSIAN PROCESS METAMODEL

2020 ◽  
Vol 10 (4) ◽  
pp. 333-349
Author(s):  
Kevin de Vries ◽  
Anna Nikishova ◽  
Benjamin Czaja ◽  
Gábor Závodszky ◽  
Alfons G. Hoekstra
Keyword(s):  
Gaussian Process ◽  
Uncertainty Quantification ◽  
Cell Model ◽  
A Cell

Preincubation with Sn-complexes causes intensive intracellular retention of 99mTc in thyroid cells in vitro

2012 ◽  
Vol 51 (05) ◽  
pp. 179-185 ◽  
Author(s):  
M. Wendisch ◽  
D. Aurich ◽  
R. Runge ◽  
R. Freudenberg ◽  
J. Kotzerke ◽  
...  
Keyword(s):  
Cell Model ◽  
Low Energy ◽  
Thyroid Cells ◽  
Low Energy Electrons ◽  
A Cell ◽  
Vitro Model ◽  
Uptake Studies ◽  
Radiobiological Effects ◽  
Radioactivity Retention

SummaryTechnetium radiopharmaceuticals are well established in nuclear medicine. Besides its well-known gamma radiation, 99mTc emits an average of five Auger and internal conversion electrons per decay. The biological toxicity of these low-energy, high-LET (linear energy transfer) emissions is a controversial subject. One aim of this study was to estimate in a cell model how much 99mTc can be present in exposed cells and which radiobiological effects could be estimated in 99mTc-overloaded cells. Methods: Sodium iodine symporter (NIS)- positive thyroid cells were used. 99mTc-uptake studies were performed after preincubation with a non-radioactive (cold) stannous pyro - phosphate kit solution or as a standard 99mTc pyrophosphate kit preparation or with pure pertechnetate solution. Survival curves were analyzed from colony-forming assays. Results: Preincubation with stannous complexes causes irreversible intracellular radioactivity retention of 99mTc and is followed by further pertechnetate influx to an unexpectedly high 99mTc level. The uptake of 99mTc pertechnetate in NIS-positive cells can be modified using stannous pyrophosphate from 3–5% to >80%. The maximum possible cellular uptake of 99mTc was 90 Bq/cell. Compared with nearly pure extracellular irradiation from routine 99mTc complexes, cell survival was reduced by 3–4 orders of magnitude after preincubation with stannous pyrophosphate. Conclusions: Intra cellular 99mTc retention is related to reduced survival, which is most likely mediated by the emission of low-energy electrons. Our findings show that the described experiments constitute a simple and useful in vitro model for radiobiological investigations in a cell model.

scholarly journals Gambogic acid protects LPS-induced apoptosis and inflammation in a cell model of neonatal pneumonia through the regulation of TrkA/Akt signaling pathway

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xu Gao ◽  
Jingya Dai ◽  
Guifang Li ◽  
Xinya Dai
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Cell Model ◽  
Akt Signaling ◽  
Gambogic Acid ◽  
Akt Signaling Pathway ◽  
Western Blot Assay ◽  
A Cell ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation

Abstract Objective In this work, we investigated the effects of gambogic acid (GA) on lipopolysaccharide (LPS)-induced apoptosis and inflammation in a cell model of neonatal pneumonia. Method Human WI-38 cells were maintained in vitro and incubated with various concentrations of GA to examine WI-38 survival. GA-preincubated WI-38 cells were then treated with LPS to investigate the protective effects of GA on LPS-induced death, apoptosis and inflammation. Western blot assay was utilized to analyze the effect of GA on tropomyosin receptor kinase A (TrkA) signaling pathway in LPS-treated WI-38 cells. In addition, human AKT serine/threonine kinase 1 (Akt) gene was knocked down in WI-38 cells to further investigate the associated genetic mechanisms of GA in protecting LPS-induced inflammation and apoptosis. Results Pre-incubating WI-38 cells with low and medium concentrations GA protected LPS-induced cell death, apoptosis and inflammatory protein productions of IL-6 and MCP-1. Using western blot assay, it was demonstrated that GA promoted TrkA phosphorylation and Akt activation in LPS-treated WI-38 cells. Knocking down Akt gene in WI-38 cells showed that GA-associated protections against LPS-induced apoptosis and inflammation were significantly reduced. Conclusions GA protected LPS-induced apoptosis and inflammation, possibly through the activations of TrkA and Akt signaling pathway. This work may broaden our understanding on the molecular mechanisms of human neonatal pneumonia.

scholarly journals Positively Charged Lipid as Potential Tool to Influence the Fate of Ethosomes

2021 ◽  
Vol 11 (15) ◽  
pp. 7060
Author(s):  
Antonia Mancuso ◽  
Maria Chiara Cristiano ◽  
Massimo Fresta ◽  
Daniele Torella ◽  
Donatella Paolino
Keyword(s):  
Cell Model ◽  
Human Keratinocytes ◽  
Skin Delivery ◽  
Physico Chemical ◽  
Cell Mortality ◽  
Mean Size ◽  
A Cell ◽  
Negative Surface ◽  
Cytotoxic Studies

Ethosomes® are one of the main deformable vesicles proposed to overcome the stratum corneum. They are composed of lecithin, ethanol and water, resulting in round vesicles characterized by a narrow size distribution and a negative surface charge. Taking into account their efficiency to deliver drugs into deeper skin layers, the current study was designed to evaluate the influence of different lipids on the physico-chemical features of traditional ethosomes in the attempt to influence their fate. Three lipids (DOPE, DSPE and DOTAP) were used for the study, but only DOTAP conferred a net positive charge to ethosomes, maintaining a narrow mean size lower than 300 nm and a good polydispersity index. Stability and in vitro cytotoxic studies have been performed using Turbiscan Lab analysis and MTT dye exclusion assay, respectively. Data recorded demonstrated the good stability of modified ethosomes and a reasonable absence of cell mortality when applied to human keratinocytes, NCTC 2544, which are used as a cell model. Finally, the best formulations were selected to evaluate their ability to encapsulate drugs, through the use of model compounds. Cationic ethosomes encapsulated oil red o and rhodamine b in amounts comparable to those recorded from conventional ethosomes (over 50%). Results recorded from this study are encouraging as cationic ethosomes may open new opportunities for skin delivery.

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