scholarly journals Epithelia–Mesenchyme Interaction Plays an Essential Role in Transdifferentiation of Retinal Pigment Epithelium of silver Mutant Quail: Localization of FGF and Related Molecules and Aberrant Migration Pattern of Neural Crest Cells during Eye Rudiment Formation

2002 ◽  
Vol 244 (2) ◽  
pp. 358-371 ◽  
Author(s):  
Masasuke Araki ◽  
Takako Takano ◽  
Tomoko Uemonsa ◽  
Yoshifumi Nakane ◽  
Masaoki Tsudzuki ◽  
...  
Keyword(s):  
Retinal Pigment Epithelium ◽  
Neural Crest ◽  
Essential Role ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Neural Crest Cells ◽  
Migration Pattern

nacre encodes a zebrafish microphthalmia-related protein that regulates neural-crest-derived pigment cell fate

Development ◽  
1999 ◽  
Vol 126 (17) ◽  
pp. 3757-3767 ◽  
Author(s):  
J.A. Lister ◽  
C.P. Robertson ◽  
T. Lepage ◽  
S.L. Johnson ◽  
D.W. Raible
Keyword(s):  
Transcription Factor ◽  
Retinal Pigment Epithelium ◽  
Neural Crest ◽  
Cell Fate ◽  
Pigment Cell ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Pigment Cells ◽  
Evolutionary Divergence ◽  
Wild Type

We report the isolation and identification of a new mutation affecting pigment cell fate in the zebrafish neural crest. Homozygous nacre (nac(w2)) mutants lack melanophores throughout development but have increased numbers of iridophores. The non-crest-derived retinal pigment epithelium is normal, suggesting that the mutation does not affect pigment synthesis per se. Expression of early melanoblast markers is absent in nacre mutants and transplant experiments suggested a cell-autonomous function in melanophores. We show that nac(w2) is a mutation in a zebrafish gene encoding a basic helix-loop-helix/leucine zipper transcription factor related to microphthalmia (Mitf), a gene known to be required for development of eye and crest pigment cells in the mouse. Transient expression of the wild-type nacre gene restored melanophore development in nacre(−/−) embryos. Furthermore, misexpression of nacre induced the formation of ectopic melanized cells and caused defects in eye development in wild-type and mutant embryos. These results demonstrate that melanophore development in fish and mammals shares a dependence on the nacre/Mitf transcription factor, but that proper development of the retinal pigment epithelium in the fish is not nacre-dependent, suggesting an evolutionary divergence in the function of this gene.

scholarly journals Neural crest cells regulate optic cup morphogenesis by promoting extracellular matrix assembly

2018 ◽  
Author(s):  
Chase D. Bryan ◽  
Rebecca L. Pfeiffer ◽  
Bryan W. Jones ◽  
Kristen M. Kwan
Keyword(s):  
Extracellular Matrix ◽  
Neural Crest ◽  
Cell Tracking ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Neural Crest Cells ◽  
Underlying Mechanism ◽  
Ultrastructural Level ◽  
Matrix Assembly ◽  
Optic Cup

AbstractThe interactions between an organ and its surrounding environment are critical in regulating its development. In vertebrates, neural crest and mesodermal mesenchymal cells have been observed close to the eye during development, and mutations affecting this periocular mesenchyme can cause defects in early eye development, yet the underlying mechanism has been unknown. Here, using timelapse microscopy and four-dimensional cell tracking in zebrafish, we establish that genetic loss of neural crest impairs cell movements within the optic vesicle. At the ultrastructural level, neural crest cells are required for basement membrane formation specifically around the retinal pigment epithelium. Neural crest cells express the extracellular matrix crosslinking protein nidogen and, strikingly, ectopically expressing nidogen in the absence of neural crest partially restores optic cup morphogenesis. These results demonstrate that the neural crest is required for local establishment of ocular extracellular matrix superstructure, which in turn drives optic cup morphogenesis.

scholarly journals Multi-ocular Organoids from Human iPS Cells Displayed Retina, Cornea, and RPE Lineages

2021 ◽  
Author(s):  
Helena Isla-Magrané ◽  
Anna Veiga ◽  
José García-Arumí ◽  
Anna Duarri
Keyword(s):  
Stem Cells ◽  
Retinal Pigment Epithelium ◽  
Epithelial Cells ◽  
Neural Crest ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Retinal Cell ◽  
Simple Method ◽  
Surface Ectoderm ◽  
Starting Point

Abstract Background: The mammalian eye is a complex organ, comprising different highly specialized tissues derived from various cell linages, including neural ectoderm, surface ectoderm, neural crest and the periocular mesenchyme. Great efforts have been made to design protocols for obtaining ocular cells from human stem cells to model diseases or for regenerative purposes, but the complex crosstalk between ocular cell types driving self-organizing growth is usually limited by restricted experimental designs. Current protocols are overall focused on the isolation of retinal, retinal pigment epithelium (RPE) or corneal cells. Here, we obtained multi-ocular organoids from human induced pluripotent stem cells. Methods: We sought to establish a simple method to induce eye field-commitment in 2D hiPSC cultures with the aim of obtaining self-organized multi-zone ocular progenitor cells in 3 weeks. From this starting point, we generated 3D multi-ocular organoids from the same culture, recapitulating important cellular features of the developing eye. Results: Self-formed multi-zone ocular progenitors in 2D culture spanned the neuroectoderm, surface ectoderm, neural crest and RPE. After manual isolation and growth in suspension, they develop into different 3D multi-ocular organoids composed of multiple cell lineages: retinal pigment epithelium, retina and cornea which could be also generated individually. Within these organoids, retinal regions display correct layering and harbor all major retinal cell subtypes as well as retinal morphological cues, whereas corneal regions closely resemble the transparent ocular-surface epithelium with characteristics of corneal, limbal and conjunctival epithelial cells. RPE also arranged to form organoids composed of polarized pigmented epithelial cells at the surface, full-filled with collagen matrix. Conclusions: The multi-ocular organoids offer a new platform to study early human eye development and disease, and provide a source of human ocular cells from the same individual.

scholarly journals Primary cilia deficiency in neural crest cells models anterior segment dysgenesis in mouse

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Céline Portal ◽  
Panteleimos Rompolas ◽  
Peter Lwigale ◽  
Carlo Iomini
Keyword(s):  
Neural Crest ◽  
Primary Cilia ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Anterior Segment ◽  
Neural Crest Cells ◽  
Corneal Neovascularization ◽  
Anterior Segment Dysgenesis ◽  
Chamber Volume ◽  
Signaling Axis

Defects affecting tissues of the anterior segment (AS) of the eye lead to a group of highly debilitating disorders called Anterior Segment Dysgenesis (ASD). Despite the identification of some causative genes, the pathogenesis of ASD remains unclear. Interestingly, several ciliopathies display conditions of the AS. Using conditional targeting of Ift88 with Wnt1-Cre, we show that primary cilia of neural crest cells (NCC), precursors of most AS structures, are indispensable for normal AS development and their ablation leads to ASD conditions including abnormal corneal dimensions, defective iridocorneal angle, reduced anterior chamber volume and corneal neovascularization. Mechanistically, NCC cilia ablation abolishes hedgehog (Hh) signaling in the periocular mesenchyme (POM) canonically activated by choroid-secreted Indian Hh, reduces proliferation of POM cells surrounding the retinal pigment epithelium and decreases the expression of Foxc1 and Pitx2, two transcription factors identified as major ASD causative genes. Thus, we uncovered a signaling axis linking cilia and ASD.

High-voltage electron microscopy of subretinal scar formation

1992 ◽  
Vol 50 (1) ◽  
pp. 486-487
Author(s):  
G.E. Korte ◽  
M. Marko ◽  
G. Hageman
Keyword(s):  
Electron Microscopy ◽  
Monoclonal Antibody ◽  
Retinal Pigment Epithelium ◽  
Glial Cells ◽  
High Voltage ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Sodium Iodate ◽  
High Voltage Electron Microscopy ◽  
Voltage Electron

Sodium iodate iv. damages the retinal pigment epithelium (RPE) in rabbits. Where RPE does not regenerate (e.g., 1,2) Muller glial cells (MC) forma subretinal scar that replaces RPE. The MC response was studied by HVEM in 3D computer reconstructions of serial thick sections, made using the STEREC0N program (3), and the HVEM at the NYS Dept. of Health in Albany, NY. Tissue was processed for HVEM or immunofluorescence localization of a monoclonal antibody recognizing MG microvilli (4).

scholarly journals 4-(Phenylsulfanyl) Butan-2-One Attenuates the Inflammatory Response Induced by Amyloid-β Oligomers in Retinal Pigment Epithelium Cells

Marine Drugs ◽  
2020 ◽  
Vol 19 (1) ◽  
pp. 1
Author(s):  
Peeraporn Varinthra ◽  
Shun-Ping Huang ◽  
Supin Chompoopong ◽  
Zhi-Hong Wen ◽  
Ingrid Y. Liu
Keyword(s):  
Retinal Pigment Epithelium ◽  
Inflammatory Response ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Amyloid Β ◽  
Age Related Macular Degeneration ◽  
Epithelial Cell Line ◽  
Age Related ◽  
Tnf Α ◽  
Cox 2

Age-related macular degeneration (AMD) is a progressive eye disease that causes irreversible impairment of central vision, and effective treatment is not yet available. Extracellular accumulation of amyloid-beta (Aβ) in drusen that lie under the retinal pigment epithelium (RPE) has been reported as one of the early signs of AMD and was found in more than 60% of Alzheimer’s disease (AD) patients. Extracellular deposition of Aβ can induce the expression of inflammatory cytokines such as IL-1β, TNF-α, COX-2, and iNOS in RPE cells. Thus, finding a compound that can effectively reduce the inflammatory response may help the treatment of AMD. In this research, we investigated the anti-inflammatory effect of the coral-derived compound 4-(phenylsulfanyl) butan-2-one (4-PSB-2) on Aβ1-42 oligomer (oAβ1-42) added to the human adult retinal pigment epithelial cell line (ARPE-19). Our results demonstrated that 4-PSB-2 can decrease the elevated expressions of TNF-α, COX-2, and iNOS via NF-κB signaling in ARPE-19 cells treated with oAβ1-42 without causing any cytotoxicity or notable side effects. This study suggests that 4-PSB-2 is a promising drug candidate for attenuation of AMD.

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