Cell death in the dorsal part of the chick optic cup. Evidence for a new necrotic area

The spatiotemporal pattern of morphogenetic cell death during the early development of the chick retina was studied by means of the neutral red vital staining and light microscopy. A modification of the conventional procedure of vital staining, which consisted of the injection of the dye into the neural tube lumen, was used for this purpose. In addition to the two areas of cell death known from previous literature, the first located in the ventral part of the optic cup and the second located in the insertion of the optic stalk with the diencephalon, a new area of cell death was described. This third necrotic area was located in the protruding dorsal part of the optic cup rim and was present throughout the stages 15 to 18. The area consisted of dying cells, fragments and phagocytosed cells. We suggest that this dorsal area of cell death could stop the intense dorsal growth of the optic cup and/or reshape the optic cup rim. Moreover, this area may influence the production of cell degeneration in the dorsal part of the invaginating lens placode.

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Interdigital tissue chondrogenesis induced by surgical removal of the ectoderm in the embryonic chick leg bud

Development ◽

10.1242/dev.94.1.231 ◽

1986 ◽

Vol 94 (1) ◽

pp. 231-244

Author(s):

J. M. Hurle ◽

Y. Gañan

Keyword(s):

Cell Death ◽

Vital Staining ◽

Mesenchymal Cell ◽

Neutral Red ◽

Surgical Removal ◽

Experimental Conditions ◽

Local Inhibition ◽

Dorsal Ectoderm ◽

Interdigital Cell Death ◽

Proximal Zone

In the present work, we have analysed the possible involvement of ectodermal tissue in the control of interdigital mesenchymal cell death. Two types of experiments were performed in the stages previous to the onset of interdigital cell death: (i) removal of the AER of the interdigit; (ii) removal of the dorsal ectoderm of the interdigit. After the operation embryos were sacrificed at 10–12h intervals and the leg buds were studied by whole-mount cartilage staining, vital staining with neutral red and scanning electron microscopy. Between stages 27 and 30, ridge removal caused a local inhibition of the growth of the interdigit. In a high percentage of the cases, ridge removal at these stages was followed 30–40 h later by the formation of ectopic nodules of cartilage in the interdigit. The incidence of ectopic cartilage formation was maximum at stage 29 (60%). In all cases, cell death took place on schedule although the intensity and extent of necrosis appeared diminished in relation to the intensity of inhibition of interdigital growth and to the presence of interdigital cartilages. Ridge removal at stage 31 did not cause inhibition of the growth of the interdigit and ectopic chondrogenesis was only detected in 3 out of 35 operated embryos. Dorsal ectoderm removal from the proximal zone of the interdigit at stage 29 caused the chondrogenesis of the proximal interdigital mesenchyme in 6 out of 18 operated embryos. The pattern of neutral red vital staining was consistent with these results revealing a partial inhibition of interdigital cell death in the proximal zone of the interdigit. It is proposed that under the present experimental conditions the mesenchymal cells are diverted from the death programme by a primary transformation into cartilage.

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Examining bivalve fecundity: oocyte viability revealed by Neutral Red vital staining

Aquaculture International ◽

10.1007/s10499-021-00686-6 ◽

2021 ◽

Author(s):

Peter G. Beninger ◽

Daphné Chérel ◽

Lucie Kessler

Keyword(s):

Vital Staining ◽

Neutral Red

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Intake of ω-6 Polyunsaturated Fatty Acid-Rich Vegetable Oils and Risk of Lifestyle Diseases

Advances in Nutrition ◽

10.1093/advances/nmaa072 ◽

2020 ◽

Vol 11 (6) ◽

pp. 1489-1509

Author(s):

Tetsumori Yamashima ◽

Tsuguhito Ota ◽

Eishiro Mizukoshi ◽

Hiroyuki Nakamura ◽

Yasuhiko Yamamoto ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Fatty Acids ◽

Cell Death ◽

Fatty Acid ◽

Vegetable Oils ◽

Neuronal Death ◽

Cell Degeneration ◽

Fried Foods ◽

Lifestyle Diseases

Abstract Although excessive consumption of deep-fried foods is regarded as 1 of the most important epidemiological factors of lifestyle diseases such as Alzheimer's disease, type 2 diabetes, and obesity, the exact mechanism remains unknown. This review aims to discuss whether heated cooking oil-derived peroxidation products cause cell degeneration/death for the occurrence of lifestyle diseases. Deep-fried foods cooked in ω-6 PUFA-rich vegetable oils such as rapeseed (canola), soybean, sunflower, and corn oils, already contain or intrinsically generate “hydroxynonenal” by peroxidation. As demonstrated previously, hydroxynonenal promotes carbonylation of heat-shock protein 70.1 (Hsp70.1), with the resultant impaired ability of cells to recycle damaged proteins and stabilize the lysosomal membrane. Until now, the implication of lysosomal/autophagy failure due to the daily consumption of ω-6 PUFA-rich vegetable oils in the progression of cell degeneration/death has not been reported. Since the “calpain-cathepsin hypothesis” was formulated as a cause of ischemic neuronal death in 1998, its relevance to Alzheimer's neuronal death has been suggested with particular attention to hydroxynonenal. However, its relevance to cell death of the hypothalamus, liver, and pancreas, especially related to appetite/energy control, is unknown. The hypothalamus senses information from both adipocyte-derived leptin and circulating free fatty acids. Concentrations of circulating fatty acid and its oxidized form, especially hydroxynonenal, are increased in obese and/or aged subjects. As overactivation of the fatty acid receptor G-protein coupled receptor 40 (GPR40) in response to excessive or oxidized fatty acids in these subjects may lead to the disruption of Ca2+ homeostasis, it should be evaluated whether GPR40 overactivation contributes to diverse cell death. Here, we describe the molecular implication of ω-6 PUFA-rich vegetable oil-derived hydroxynonenal in lysosomal destabilization leading to cell death. By oxidizing Hsp70.1, both the dietary PUFA- (exogenous) and the membrane phospholipid- (intrinsic) peroxidation product “hydroxynonenal,” when combined, may play crucial roles in the occurrence of diverse lifestyle diseases including Alzheimer's disease.

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VITAL STAINING PROPERTIES OF NEUTRAL RED

Acta Ophthalmologica ◽

10.1111/j.1755-3768.1978.tb06638.x ◽

2009 ◽

Vol 56 (5) ◽

pp. 742-750 ◽

Cited By ~ 3

Author(s):

KIRSTEN MARNER ◽

MOGENS S. NORN

Keyword(s):

Vital Staining ◽

Neutral Red

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413. Differences in Inflammatory Mechanisms in Pseudomonas aeruginosa and Staphyloccoccus auereus Infections in Cystic Fibrosis

Open Forum Infectious Diseases ◽

10.1093/ofid/ofz360.486 ◽

2019 ◽

Vol 6 (Supplement_2) ◽

pp. S209-S209

Author(s):

Melissa S Phuong ◽

Rafael E Hernandez ◽

Subash Sad

Keyword(s):

Cystic Fibrosis ◽

Pseudomonas Aeruginosa ◽

Cell Death ◽

Cytokine Production ◽

Neutral Red ◽

Chronic Infections ◽

Neutral Red Assay ◽

The One ◽

The University

Abstract Background Chronic bacterial lung infections are the primary cause of morbidity and mortality in cystic fibrosis (CF). The most common CF pathogens, Pseudomonas aeruginosa (P. aeruginosa) or Staphylococcus aureus (S. aureus), are common commensal or environmental organisms that adapt to the CF lung. We sought to investigate whether adaptation from early lung colonizer to chronic pathogen alters the bacterial effects on host inflammation. Methods P. aeruginosa (n = 25) and S. aureus (n = 25) isolates from CF patients with early and chronic infections were acquired from Seattle Children’s CF. Environmental (n = 8) and clinical, non-CF P. aeruginosa (n = 8) isolates were obtained from the University of Ottawa. P. aeruginosa reference strain PA14 and PA14 transposon mutants for T3SS and flagellin were used to observe the relationship between cell death and cytokine production. We infected THP-1-derived macrophages (PMA differentiated) in vitro for 3 hours with various MOIs. We subsequently measured cell death of THP-1-derived macrophages using neutral red assay and cytokine production using ELISAs. Results Infections with PA14 mutants and non-CF P. aeruginosa isolates demonstrated that rapid cell death of THP-1-derived macrophages caused a reduction in cytokine production relative to strains that did not cause as much cell death. At 10 MOI, early P. aeruginosa isolates from CF patients induced more THP-1-derived macrophage cell death compared with chronic isolates (P < 0.0001). Chronic P. aeruginosa isolates induced greater production of TNF, IL-8, and IL-6 (P < 0.01, P < 0.0001, and P < 0.0001, respectively) compared with early strains. No difference in IL-1β production was observed. When controlling for cell death between the two groups by using heat-killed bacteria, the only difference maintained was in TNF production (P < 0.01). Between early and chronic S. aureus isolates, the one difference observed was greater IL-8 production among early isolates (P < 0.01). Conclusion Chronic P. aeruginosa isolates from CF patients induce less cell death but more TNF, IL-8, and IL-6 production compared with early isolates. This suggests that P. aeruginosa producing chronic infections induce inflammatory signals that may contribute to increased morbidity among CF patients. Disclosures All authors: No reported disclosures.

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Apoptosis, retinitis pigmentosa, and degeneration

Biochemistry and Cell Biology ◽

10.1139/o94-066 ◽

1994 ◽

Vol 72 (11-12) ◽

pp. 489-498 ◽

Cited By ~ 48

Author(s):

Paul Wong

Keyword(s):

Cell Death ◽

Retinitis Pigmentosa ◽

Retinal Degeneration ◽

Photoreceptor Cell ◽

Retinal Cell ◽

Current Evidence ◽

Cell Degeneration ◽

Genetic Lesion ◽

Common Causes ◽

Active Cell Death

The mechanism of photoreceptor cell death in different inherited retinal degenerations is not fully understood. Mutations in a number of different genes (such as rhodopsin, the beta subunit of cGMP phosphodiesterase, and peripherin) have been identified as the primary genetic lesion in different forms of human retinitis pigmentosa, one of the most common causes of inherited blindness. In all cases the manifestation of the disorder regardless of the specific primary genetic lesion is similar, resulting in photoreceptor cell degeneration and blindness. A recent hypothesis is that the active photoreceptor cell death, which is characteristic of these genetically distinct disorders, is mediated by a common induction of apoptosis. In the present review, the current evidence for active cell death during retinal cell death in several different rodent models of retinitis pigmentosa and retinal degeneration is examined.Key words: retinal degeneration, apoptosis, retinitis pigmentosa, clusterin, DNA fragmentation.

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Transforming growth factor-β induced cell death in the developing chick retina is mediated via activation of c-jun N-terminal kinase and downregulation of the anti-apoptotic protein Bcl-XL

Neuroscience Letters ◽

10.1016/s0304-3940(02)00801-7 ◽

2002 ◽

Vol 330 (3) ◽

pp. 239-242 ◽

Cited By ~ 9

Author(s):

Norbert Schuster ◽

Nicole Dünker ◽

Kerstin Krieglstein

Keyword(s):

Cell Death ◽

Growth Factor ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Chick Retina ◽

Apoptotic Protein

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Analysis of Programmed Cell Death and Senescence Markers in the Developing Retina of an Altricial Bird Species

Cells ◽

10.3390/cells10030504 ◽

2021 ◽

Vol 10 (3) ◽

pp. 504

Author(s):

Guadalupe Álvarez-Hernán ◽

José Antonio de Mera-Rodríguez ◽

Ismael Hernández-Núñez ◽

Alfonso Marzal ◽

Yolanda Gañán ◽

...

Keyword(s):

Cell Death ◽

Optic Nerve ◽

Programmed Cell Death ◽

Central Region ◽

Optic Nerve Head ◽

Bird Species ◽

Distribution Patterns ◽

Photoreceptor Layer ◽

Optic Cup ◽

Small Focus

This study shows the distribution patterns of apoptotic cells and biomarkers of cellular senescence during the ontogeny of the retina in the zebra finch (T. guttata). Neurogenesis in this altricial bird species is intense in the retina at perinatal and post-hatching stages, as opposed to precocial bird species in which retinogenesis occurs entirely during the embryonic period. Various phases of programmed cell death (PCD) were distinguishable in the T. guttata visual system. These included areas of PCD in the central region of the neuroretina at the stages of optic cup morphogenesis, and in the sub-optic necrotic centers (St15–20). A small focus of early neural PCD was detected in the neuroblastic layer, dorsal to the optic nerve head, coinciding with the appearance of the first differentiated neuroblasts (St24–St25). There were sparse pyknotic bodies in the non-laminated retina between St26 and St37. An intense wave of neurotrophic PCD was detected in the laminated retina between St42 and P8, the last post-hatching stage included in the present study. PCD was absent from the photoreceptor layer. Phagocytic activity was also detected in Müller cells during the wave of neurotrophic PCD. With regard to the chronotopographical staining patterns of senescence biomarkers, there was strong parallelism between the SA-β-GAL signal and p21 immunoreactivity in both the undifferentiated and the laminated retina, coinciding in the cell body of differentiated neurons. In contrast, no correlation was found between SA-β-GAL activity and the distribution of TUNEL-positive cells in the developing tissue.

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