scholarly journals A protocol to evaluate epithelial regeneration after inducing cell loss in zebrafish larvae

2022 ◽  
Vol 3 (1) ◽  
pp. 101073
Author(s):  
Oscar E. Ruiz ◽  
Krystin M. Samms ◽  
George T. Eisenhoffer
Keyword(s):  
Cell Loss ◽  
Epithelial Regeneration ◽  
Zebrafish Larvae

scholarly journals Role of metaplasia during gastric regeneration

2020 ◽  
Vol 319 (6) ◽  
pp. C947-C954
Author(s):  
Emma Teal ◽  
Martha Dua-Awereh ◽  
Sabrina T. Hirshorn ◽  
Yana Zavros
Keyword(s):  
Cell Proliferation ◽  
Glutamate Transporter ◽  
Cell Loss ◽  
Redox Balance ◽  
Gastric Epithelium ◽  
Gastric Injury ◽  
M2 Macrophage ◽  
Cd44 Variant ◽  
Epithelial Regeneration

Spasmolytic polypeptide/trefoil factor 2 (TFF2)-expressing metaplasia (SPEM) is a mucous-secreting reparative lineage that emerges at the ulcer margin in response to gastric injury. Under conditions of chronic inflammation with parietal cell loss, SPEM has been found to emerge and evolve into neoplasia. Cluster-of-differentiation gene 44 (CD44) is known to coordinate normal and metaplastic epithelial cell proliferation. In particular, CD44 variant isoform 9 (CD44v9) associates with the cystine-glutamate transporter xCT, stabilizes the protein, and provides defense against reactive oxygen species (ROS). xCT stabilization by CD44v9 leads to defense against ROS by cystine uptake, glutathione (GSH) synthesis, and maintenance of the redox balance within the intracellular environment. Furthermore, p38 signaling is a known downstream ROS target, leading to diminished cell proliferation and migration, two vital processes of gastric epithelial repair. CD44v9 emerges during repair of the gastric epithelium after injury, where it is coexpressed with other markers of SPEM. The regulatory mechanisms for the emergence of CD44v9 and the role of CD44v9 during the process of gastric epithelial regeneration are largely unknown. Inflammation and M2 macrophage infiltration have recently been demonstrated to play key roles in the induction of SPEM after injury. The following review proposes new insights into the functional role of metaplasia in the process of gastric regeneration in response to ulceration. Our insights are extrapolated from documented studies reporting oxyntic atrophy and SPEM development and our current unpublished findings using the acetic acid-induced gastric injury model.

scholarly journals Comprehensive Analysis of Neurotoxin-Induced Ablation of Dopaminergic Neurons in Zebrafish Larvae

Biomedicines ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 1 ◽  
Author(s):  
Michael Kalyn ◽  
Khang Hua ◽  
Suzita Mohd Noor ◽  
Chee Ern David Wong ◽  
Marc Ekker
Keyword(s):  
Dopaminergic Neurons ◽  
Cell Loss ◽  
Motor Deficit ◽  
Transgenic Zebrafish ◽  
Larval Zebrafish ◽  
Zebrafish Larvae ◽  
High Throughput Drug Screening ◽  
Gene Expression Analyses ◽  
Substantial Degree ◽  
Ventral Diencephalon

Neurotoxin exposure of zebrafish larvae has been used to mimic a Parkinson’s disease (PD) phenotype and to facilitate high-throughput drug screening. However, the vulnerability of zebrafish to various neurotoxins was shown to be variable. Here, we provide a direct comparison of ablative effectiveness in order to identify the optimal neurotoxin-mediated dopaminergic (DAnergic) neuronal death in larval zebrafish. Transgenic zebrafish, Tg(dat:eGFP), were exposed to different concentrations of the neurotoxins MPTP, MPP+, paraquat, 6-OHDA, and rotenone for four days, starting at three days post-fertilization. The LC50 of each respective neurotoxin concentration was determined. Confocal live imaging on Tg(dat:eGFP) showed that MPTP, MPP+, and rotenone caused comparable DAnergic cell loss in the ventral diencephalon (vDC) region while, paraquat and 6-OHDA caused fewer losses of DAnergic cells. These results were further supported by respective gene expression analyses of dat, th, and p53. Importantly, the loss of DAnergic cells from exposure to MPTP, MPP+, and rotenone impacted larval locomotor function. MPTP induced the largest motor deficit, but this was accompanied by the most severe morphological impairment. We conclude that, of the tested neurotoxins, MPP+ recapitulates a substantial degree of DAnergic ablation and slight locomotor perturbations without systemic defects indicative of a Parkinsonian phenotype.

scholarly journals Evaluation of Ototoxicity of an Antifog Agent and the Suspected Underlying Mechanisms: An Animal Study

2019 ◽  
Vol 98 (9) ◽  
pp. NP131-NP137
Author(s):  
Jihye Rhee ◽  
Eunjung Han ◽  
Yoon Chan Rah ◽  
Saemi Park ◽  
Soonil Koun ◽  
...  
Keyword(s):  
Hair Cell ◽  
Middle Ear ◽  
Hair Cells ◽  
Cell Damage ◽  
Cell Loss ◽  
Control Group ◽  
Hair Cell Loss ◽  
Zebrafish Larvae ◽  
Hair Cell Damage ◽  
Underlying Mechanisms

Use of rigid endoscopes has become widespread in middle ear surgeries, thereby attracting attention to the safety of antifog agents. However, few studies on the ototoxicity of antifog agents have been conducted. The purpose of this study was to evaluate hair cell damage and the underlying mechanisms caused by antifog agents using zebrafish larvae. We exposed zebrafish larvae at 3 days postfertilization to various concentrations of the antifog agent, Ultrastop (0.01, 0.02, 0.04, and 0.08%) for 72 hours. The average number of hair cells within 4 neuromasts of larvae, including supraorbital (SO1 and SO2), otic (O1), and occipital (OC1), in the control group were compared to those in the exposure groups. Significant hair cell loss was observed in the experimental groups compared to that in the control group ( P < .01; control: 53.88 ± 4.85, 0.01%: 45.08 ± 11.70, 0.02%: 41.36 ± 12.00, 0.04%: 35.36 ± 16.18, and 0.08%: 15.60 ± 7.53 cells). Concentration-dependent increase in hair cell apoptosis by terminal deoxynucleotidyltransferase (TDT)-mediated dUTP-biotin nick end labeling assay (control: 0.00 ± 0.00, 0.01%: 3.48 ± 2.18, 0.02%: 9.64 ± 5.75, 0.04%: 17.72 ± 6.26, and 0.08%: 14.60 ± 8.18 cells) and decrease in the viability of hair cell mitochondria by 2-(4-[dimethylamino] styryl)-N-ethylpyridinium iodide assay (control: 9.61 ± 1.47, 0.01%: 8.28 ± 2.22, 0.02%: 8.45 ± 2.72, 0.04%: 7.25 ± 2.44, and 0.08%: 6.77 ± 3.26 percentage of total area) were observed. Antifog agent exposure can cause hair cell damage in zebrafish larvae, possibly by induction of mitochondrial damage with subsequent apoptosis of hair cells.

Generation of Clara cells from murine pluripotent stem cells – a new tool to explore airway epithelial regeneration

Pneumologie ◽  
2014 ◽  
Vol 68 (06) ◽  
Author(s):  
K Katsirntaki ◽  
C Mauritz ◽  
S Schmeckebier ◽  
M Sgodda ◽  
V Puppe ◽  
...  
Keyword(s):  
Stem Cells ◽  
Pluripotent Stem Cells ◽  
Airway Epithelial ◽  
Clara Cells ◽  
Epithelial Regeneration

Strahlenwirkung am Normalgewebe

2010 ◽  
Vol 49 (S 01) ◽  
pp. S53-S58 ◽  
Author(s):  
W. Dörr
Keyword(s):  
Radiation Exposure ◽  
Normal Tissue ◽  
Radiation Effects ◽  
A Priori ◽  
Cell Loss ◽  
Turnover Time ◽  
Complete Healing ◽  
Internal Radiotherapy ◽  
Normal Tissues ◽  
Chronic Radiation

SummaryThe curative effectivity of external or internal radiotherapy necessitates exposure of normal tissues with significant radiation doses, and hence must be associated with an accepted rate of side effects. These complications can not a priori be considered as an indication of a too aggressive therapy. Based on the time of first diagnosis, early (acute) and late (chronic) radiation sequelae in normal tissues can be distinguished. Early reactions per definition occur within 90 days after onset of the radiation exposure. They are based on impairment of cell production in turnover tissues, which in face of ongoing cell loss results in hypoplasia and eventually a complete loss of functional cells. The latent time is largely independent of dose and is defined by tissue biology (turnover time). Usually, complete healing of early reactions is observed. Late radiation effects can occur after symptom-free latent times of months to many years, with an inverse dependence of latency on dose. Late normal tissue changes are progressive and usually irreversible. They are based on a complex interaction of damage to various cell populations (organ parenchyma, connective tissue, capillaries), with a contribution from macrophages. Late effects are sensitive for a reduction in dose rate (recovery effects).A number of biologically based strategies for protection of normal tissues or for amelioration of radiation effects was and still is tested in experimental systems, yet, only a small fraction of these approaches has so far been introduced into clinical studies. One advantage of most of the methods is that they may be effective even if the treatment starts way after the end of radiation exposure. For a clinical exploitation, hence, the availability of early indicators for the progression of subclinical damage in the individual patient would be desirable. Moreover, there is need to further investigate the molecular pathogenesis of normal tissue effects in more detail, in order to optimise biology based preventive strategies, as well as to identify the precise mechanisms of already tested approaches (e. g. stem cells).

The identification of diabetes genes mediating β-cell loss and hyperglycemia using positional cloning

2018 ◽  
Author(s):  
TT Cui ◽  
N Hallahan ◽  
W Jonas ◽  
P Gottmann ◽  
M Jähnert ◽  
...  
Keyword(s):  
Positional Cloning ◽  
Cell Loss ◽  
Β Cell

Leucocytes and Thrombosis

1973 ◽  
Vol 30 (01) ◽  
pp. 036-046 ◽  
Author(s):  
D.C Banks ◽  
J.R.A Mitchell
Keyword(s):  
Cell Count ◽  
White Cell Count ◽  
Cell Loss ◽  
White Cell ◽  
Structural Resemblance ◽  
The Masses

SummaryWhen heparinised blood is rotated in a glass flask at 37°C. the white cell count falls and it has been shown that this is due to the adherence and aggregation of polymorphonuclear white cells on the wall of the flask. The masses formed bear a close structural resemblance to thrombi and the mechanisms involved in white cell loss during rotation may therefore increase our knowledge of the thrombotic process.

Smooth Muscle Proliferation in Chronically Injured Canine Pulmonary Arteries Is Reduced by a Potent Platelet Aggregation Inhibitor U-53,059

1985 ◽  
Vol 53 (03) ◽  
pp. 351-355 ◽  
Author(s):  
Robert G Schaub ◽  
James C Keith ◽  
Carol A Simmons ◽  
Clarence A Rawlings
Keyword(s):  
Smooth Muscle ◽  
Platelet Aggregation ◽  
Dirofilaria Immitis ◽  
Leukocyte Adhesion ◽  
Pulmonary Arteries ◽  
Cell Loss ◽  
Endothelial Cell Loss ◽  
Dense Granules ◽  
Smooth Muscle Proliferation ◽  
Aggregation Inhibitor

Summary Dirofilaria immitis (DI) infection chronically injures canine pulmonary arteries. This injury produces endothelial cell loss, platelet/leukocyte adhesion, and smooth muscle proliferation. In the present study we assessed the effect of the cyclooxygenase inhibitor, U-53,059, on platelet function, platelet kinetics, coagulation, and smooth muscle proliferation in DI infected dogs.Platelet aggregation to the combination of arachidonic acid/ ADP was significantly inhibited by U-53,059. Coagulation and hematologic parameters were not effected by either DI infection or U-53,059 treatment. Platelet survival and the number of platelet dense granules were reduced in DI infection. Quantification of the lesions demonstrated that U-53,059 reduced both severity and density compared to non-treated dogs. U-53,059 is a potent and effective inhibitor of platelet aggregation which modifies smooth muscle proliferation produced by chronic vascular injury.

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