Huperzine a provides neuroprotection against several cell death inducers usingin vitro model systems of motor neuron cell death

2008 ◽  
Vol 13 (1) ◽  
pp. 49-61 ◽  
Author(s):  
Richelle A. Hemendinger ◽  
Edward J. Armstrong ◽  
Rafal Persinski ◽  
Julianne Todd ◽  
Jean-Luc Mougeot ◽  
...  
Keyword(s):  
Cell Death ◽  
Motor Neuron ◽  
Huperzine A ◽  
Model Systems ◽  
Vitro Model

scholarly journals PACAP Modulates the Autophagy Process in an In Vitro Model of Amyotrophic Lateral Sclerosis

2020 ◽  
Vol 21 (8) ◽  
pp. 2943 ◽  
Author(s):  
Agata Grazia D’Amico ◽  
Grazia Maugeri ◽  
Salvatore Saccone ◽  
Concetta Federico ◽  
Sebastiano Cavallaro ◽  
...  
Keyword(s):  
Cell Death ◽  
Amyotrophic Lateral Sclerosis ◽  
Motor Neuron ◽  
Motor Neurons ◽  
In Vitro Model ◽  
Erk Signaling ◽  
Hypoxic Stress ◽  
Vitro Model ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease of complex etiology leading to motor neuron degeneration. Many gene alterations cause this pathology, including mutation in Cu, Zn superoxide dismutase (SOD1), which leads to its gain of function. Mutant SOD1 proteins are prone to aberrant misfolding and create aggregates that impair autophagy. The hypoxic stress is strictly linked to the disease progression since it induces uncontrolled autophagy activation and the consequent high rates of cell death. Previously, we showed that pituitary adenylate cyclase-activating polypeptide (PACAP) exerts neurotrophic activity in cultured mSOD1 motor neurons exposed to serum deprivation. To date, no studies have examined whether the protective effect of PACAP on mSOD1 cells exposed to hypoxic insult is mediated through the regulation of the autophagy process. In the present study, we used the neuroblastoma-spinal cord-34 (NSC-34) cell line, stably expressing human wild type or mutant SOD1 G93A, to represent a well characterized in vitro model of a familial form of ALS. These cells were exposed to 100-µM desferrioxamine mesylate salt for 24h, to mimic the hypoxic stress affecting motor neurons during the disease progression. Our results showed that PACAP treatment significantly reduced cell death and hypoxia-induced mSOD1 accumulation by modulating the autophagy process in G93A motor neurons, as revealed by the decreased LC3II and the increased p62 levels, two autophagy indicators. These results were also confirmed by evaluating the vacuole formation detected through light chain 3 (LC3) immunofluorescence. Furthermore, the PACAP effects on autophagy seem to be mediated through the activation of the MAPK/ERK signaling pathway. Overall, our data demonstrated that PACAP exerts an ameliorative effect on the mSOD1 motor neuron viability by modulating a hypoxia-induced autophagy process through activation of MAPK/ERK signaling cascade.

Human 3-dimensional liver organoids: in vitro model systems to study liver diseases

2020 ◽  
Author(s):  
H Gaitantzi ◽  
C Cai ◽  
S Asawa ◽  
K Böttcher ◽  
M Ebert ◽  
...  
Keyword(s):  
Liver Diseases ◽  
In Vitro Model ◽  
Model Systems ◽  
3 Dimensional ◽  
Vitro Model ◽  
Liver Organoids

scholarly journals In Vitro Model Systems for Exploring Oral Biofilms: From Single‐Species Populations to Complex Multi‐Species Communities

2021 ◽  
Author(s):  
Ting L. Luo ◽  
Michael E. Vanek ◽  
Carlos Gonzalez‐Cabezas ◽  
Carl F. Marrs ◽  
Betsy Foxman ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Single Species ◽  
Model Systems ◽  
Oral Biofilms ◽  
Vitro Model

The Human Leukemic HL-60 Cell Line: An in Vitro Model for Cell Death Endpoint Identification

1996 ◽  
Vol 24 (4) ◽  
pp. 581-587
Author(s):  
Cristiana Zanetti ◽  
Arrnalaura Stammati ◽  
Orazio Sapora ◽  
Flavia Zucco
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
In Vitro Model ◽  
Leukemia Cell ◽  
Promyelocytic Leukemia ◽  
Leukemia Cell Line ◽  
Cell Type ◽  
Vitro Model ◽  
Promyelocytic Leukemia Cell Line

The aim of this study was to investigate the endpoints related to cell death, either necrosis or apoptosis, induced by four chemicals in the promyelocytic leukemia cell line, HL-60. Cell morphology, DNA fragmentation, cytofluorimetric analysis and oxygen consumption were used to classify the type of cell death observed. In our analysis, we found that not all the selected parameters reproduced the differences observed in the cell death caused by the four chemicals tested. As cell death is a very complex phenomenon, several factors should be taken into account (cell type, exposure time and chemical concentration), if chemicals are to be classified according to differences in the mechanisms more directly involved in cell death.

scholarly journals Establishment and Characterization of an In Vitro Model of Fas-Mediated Hepatocyte Cell Death

2014 ◽  
pp. 95-103
Author(s):  
Mathieu Vinken ◽  
Michaël Maes ◽  
Sara Crespo Yanguas ◽  
Joost Willebrords ◽  
Tamara Vanhaecke ◽  
...  
Keyword(s):  
Cell Death ◽  
In Vitro Model ◽  
Vitro Model

scholarly journals Induced Human Intestinal Organoids (iHIOs) as Model Systems for Chemotherapy-associated Clostridium difficile (CD) Infections

2017 ◽  
Vol 4 (suppl_1) ◽  
pp. S382-S382
Author(s):  
Senu Apewokin ◽  
Suman Pradhan ◽  
Michael Frerick ◽  
Alison Weiss
Keyword(s):  
Cell Death ◽  
Clostridium Difficile ◽  
Experimental Models ◽  
Cytotoxic Chemotherapy ◽  
Model Systems ◽  
Epithelial Barrier ◽  
Histological Changes ◽  
Human Dose ◽  
Therapeutic Doses ◽  
Pathophysiologic Mechanisms

Abstract Background Patients undergoing cytotoxic chemotherapy are ten times more likely to develop Clostridium difficile infections (CDI) than the general patient population. Efforts to outline pathophysiologic mechanisms underlying this disproportionate incidence have been limited by the lack of disease-representative experimental models. We hypothesized that iHIOs could serve as toxicity models to evaluate chemotherapy-associated CDI Methods Intact iHIOs were exposed to cytotoxic chemotherapy (melphalan) in gut media at therapeutic doses (9 μg/mL; which is the equivalent of 140 mg/m2 human dose). Cellular death was assessed by accumulation of the membrane permeant dye, Sytox-orange added at 5-days post treatment. iHIOs were also exposed to CD toxin A and B (TcdA and TcdB respectively) and epithelial barrier damage assessed by actin mislocalization and loss of E-cadherin. For controls iHIOs were exposed / microinjected with saline/PBS. Morphological and histological changes were then captured using light and confocal microscopy Results Morphologic and histologic assessments demonstrated cell death and epithelial barrier damage Conclusion iHIOs demonstrate cell death on exposure to CD toxins and melphalan chemotherapy. These properties could be harnessed in establishing toxicity models for evaluation of chemotherapy-associated CDI Disclosures S. Apewokin, T2 biosystems: Investigator, Research support Astellas: Scientific Advisor, Consulting fee

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