scholarly journals Protocol for fungal infection following the induction of epithelial cell loss in larval zebrafish

2021 ◽  
Vol 2 (4) ◽  
pp. 100963
Author(s):  
Sebastian Wurster ◽  
Oscar E. Ruiz ◽  
Alexander M. Tatara ◽  
Dimitrios P. Kontoyiannis ◽  
George T. Eisenhoffer
Keyword(s):  
Epithelial Cell ◽  
Fungal Infection ◽  
Cell Loss ◽  
Larval Zebrafish

Cell cycle kinetics in the alveolar epithelium

1997 ◽  
Vol 272 (6) ◽  
pp. L1031-L1045 ◽  
Author(s):  
B. D. Uhal
Keyword(s):  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelium ◽  
Cell Loss ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Pathological Conditions ◽  
Type Ii Cell ◽  
The Relationship

The type II alveolar epithelial cell has important metabolic and biosynthetic functions but also serves as the stem cell of the alveolar epithelium. Much of the evidence underlying this premise was obtained before 1980 and provided the basis for a working model that has not been reconsidered for more than fifteen years. With the exceptions to be discussed below, little evidence has accumulated in the interim to suggest that the model requires significant alteration. Important questions remain unanswered, however, and some components of the model need to be supplemented, particularly in light of recent investigations that have provided insights not possible in earlier work. In particular, in vitro studies have suggested that the relationship between the parent type II cell and its progeny may not be as straightforward as originally thought. In addition, the rate of epithelial cell loss was recognized long ago to be an important factor in the regulation of this system, but its kinetics and mechanisms have received little attention. These and other unresolved issues are critical to our understanding of the homeostasis of the alveolar epithelium under normal and pathological conditions.

Human ESC–derived retinal epithelial cell sheets potentiate rescue of photoreceptor cell loss in rats with retinal degeneration

2017 ◽  
Vol 9 (421) ◽  
pp. eaai7471 ◽  
Author(s):  
Karim Ben M’Barek ◽  
Walter Habeler ◽  
Alexandra Plancheron ◽  
Mohamed Jarraya ◽  
Florian Regent ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Retinal Degeneration ◽  
Photoreceptor Cell ◽  
Cell Loss ◽  
Cell Sheets

Effects of Water-Immersion Restraint Stress on Rat Gastric Epithelial Cell Loss and Migration

1988 ◽  
Vol 10 ◽  
pp. S78-83S ◽  
Author(s):  
Hajime Kuwayama ◽  
Katsuhiro Takeuchi ◽  
Etsu Kohashi ◽  
Shinji Yoshizu ◽  
Yoshinori Tashiro ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Restraint Stress ◽  
Water Immersion ◽  
Cell Loss ◽  
Gastric Epithelial Cell ◽  
Water Immersion Restraint Stress ◽  
And Migration

Fibronectin fragments induce MMP activity in mouse mammary epithelial cells: evidence for a role in mammary tissue remodeling

2000 ◽  
Vol 113 (5) ◽  
pp. 795-806 ◽  
Author(s):  
P. Schedin ◽  
R. Strange ◽  
T. Mitrenga ◽  
P. Wolfe ◽  
M. Kaeck
Keyword(s):  
Extracellular Matrix ◽  
Mammary Gland ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Protease Activity ◽  
Mammary Epithelial Cells ◽  
Cell Loss ◽  
Mammary Epithelial ◽  
Epithelial Cell Line ◽  
Fibronectin Fragments

Mammary gland form and function are regulated by interactions between epithelium and extracellular matrix. Major glycoprotein components of extracellular matrix have been identified that give survival, proliferation and differentiation signals to mammary epithelial cells. We provide evidence that proteolytic fragments of the extracellular matrix glycoprotein, fibronectin, suppress growth and can promote apoptosis of mouse mammary epithelial cells. During mammary gland involution, total fibronectin and fibronectin fragment levels are increased. The peak levels of fibronectin protein and fragments are observed 4–6 days post-weaning, coincident with the peak in epithelial cell death. Using a model for hormone withdrawal-induced death of mammary epithelium, elevated levels of fibronectin proteolytic fragments were associated with apoptosis in TM-6 cells, a tumorigenic mouse mammary epithelial cell line. Treatment of TM-6 cells with exogenous fibronectin fragments (FN120) reduced cell number, and induced apoptosis and matrix degrading protease activity. Inhibition of matrix protease activity rescued TM-6 cell viability, indicating that FN120-induced cell loss is mediated through matrix protease activity. In a three-dimensional model for mammary gland development, FN120 reduced alveolar-like and promoted ductal-like development by a matrix protease-dependent mechanism. These data suggest that during post-lactational involution, fibronectin fragments may contribute to epithelial cell loss and dissolution of mammary alveoli by inducing matrix degrading proteinases.

Tissue economics of hydra: regulation of cell cycle, animal size and development by controlled feeding rates

1977 ◽  
Vol 28 (1) ◽  
pp. 117-132
Author(s):  
J.J. Otto ◽  
R.D. Campbell
Keyword(s):  
Cell Cycle ◽  
Steady State ◽  
Epithelial Cell ◽  
Cycle Time ◽  
Cell Loss ◽  
Tissue Growth ◽  
Tissue Loss ◽  
Feeding Rates ◽  
Cell Cycle Time ◽  
Steady State Condition

Epithelial cell production and epithelial cell loss in 6 different size classes of Hydra attenuata were examined to understand the relationships between growth and morphogenesis. The sizes of adult hydra, the sizes of their buds, and their budding rates are all nearly proportional to the amount of food the hydra eat. Hydra fed at high rates (4-25 Artemia nauplii per day) all have the same epithelial cell cycle time (about 4 days). Budding accounts for most of their cell loss. Hydra fed 4–12 Artemia per day maintain a steady state condition in which tissue loss balances tissue growth. Animals fed 25 Artemia per day are not in a steady state growth condition and change in size. At the lowest feeding rates (0-1 Artemia per day), the epithelial cell cycle time is lengthened to about 16 days. Cell loss from the tentacles accounts for most of the cell loss, and this loss is not completely balanced by growth. As a consequence these animals cease budding and shrink in size.

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.

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