Fate of Corneal Epithelial Cells Separated from Limbus In Vivo

2011 ◽  
Vol 52 (11) ◽  
pp. 8132 ◽  
Author(s):  
Tetsuya Kawakita ◽  
Kazunari Higa ◽  
Shigeto Shimmura ◽  
Machiko Tomita ◽  
Kazuo Tsubota ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial

scholarly journals The core planar cell polarity gene, Vangl2 , directs adult corneal epithelial cell alignment and migration

2016 ◽  
Vol 3 (10) ◽  
pp. 160658 ◽  
Author(s):  
Amy S. Findlay ◽  
D. Alessio Panzica ◽  
Petr Walczysko ◽  
Amy B. Holt ◽  
Deborah J. Henderson ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cells ◽  
Cell Polarity ◽  
Corneal Epithelium ◽  
Planar Cell Polarity ◽  
Corneal Epithelial Cell ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
The Core

This study shows that the core planar cell polarity (PCP) genes direct the aligned cell migration in the adult corneal epithelium, a stratified squamous epithelium on the outer surface of the vertebrate eye. Expression of multiple core PCP genes was demonstrated in the adult corneal epithelium. PCP components were manipulated genetically and pharmacologically in human and mouse corneal epithelial cells in vivo and in vitro . Knockdown of VANGL2 reduced the directional component of migration of human corneal epithelial (HCE) cells without affecting speed. It was shown that signalling through PCP mediators, dishevelled, dishevelled-associated activator of morphogenesis and Rho-associated protein kinase directs the alignment of HCE cells by affecting cytoskeletal reorganization. Cells in which VANGL2 was disrupted tended to misalign on grooved surfaces and migrate across, rather than parallel to the grooves. Adult corneal epithelial cells in which Vangl2 had been conditionally deleted showed a reduced rate of wound-healing migration. Conditional deletion of Vangl2 in the mouse corneal epithelium ablated the normal highly stereotyped patterns of centripetal cell migration in vivo from the periphery (limbus) to the centre of the cornea. Corneal opacity owing to chronic wounding is a major cause of degenerative blindness across the world, and this study shows that Vangl2 activity is required for directional corneal epithelial migration.

scholarly journals In Vivo Confocal Microscopy of Cornea in Patients with Terrien’s Marginal Corneal Degeneration

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Ting Chen ◽  
Qiangxiang Li ◽  
Xiangbo Tang ◽  
Min Liao ◽  
Hua Wang
Keyword(s):  
Epithelial Cells ◽  
Confocal Microscopy ◽  
Stromal Cells ◽  
Nerve Fibers ◽  
In Vivo Confocal Microscopy ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Department Of Ophthalmology ◽  
Severity Of The Disease

This study was aimed at observing the morphological changes of the cornea with ocular in vivo confocal microscopy (IVCM) in patients with Terrien’s marginal degeneration (TMD). Ten patients (20 eyes) with TMD treated in the Department of Ophthalmology, Xiangya Hospital, and 10 healthy controls (20 eyes) were included in the current study. A detailed slit lamp microscopy, anterior segment photography, and corneal IVCM examination were performed for each eye. The density of central and marginal corneal epithelial cells, stromal cells, and subepithelial nerve fibers was compared between the two groups using the Wilcoxon rank sum test. Compared with the control group, the corneal epithelial and endothelial cells in the TMD group showed granular highly reflective substances and thinner subepithelial nerve fibers. The uneven dot-like highly reflective substances without cell structures appeared in the stromal layer of the cornea. The density of central and marginal corneal epithelial cells, stromal cells, and subepithelial nerve fibers was lower in the TMD group (p<0.05), and they were negatively correlated with severity of the disease (p<0.05). Our study demonstrated that the density of corneal epithelial cells, stromal cells, and sensory plexus nerve fibers was significantly reduced in the TMD group. The pathological changes were more obvious in the marginal cornea, and it is correlated with severity of the disease.

scholarly journals Interferon-γ-induced MD-2 Protein Expression and Lipopolysaccharide (LPS) Responsiveness in Corneal Epithelial Cells Is Mediated by Janus Tyrosine Kinase-2 Activation and Direct Binding of STAT1 Protein to the MD-2 Promoter

2011 ◽  
Vol 286 (27) ◽  
pp. 23753-23762 ◽  
Author(s):  
Sanhita Roy ◽  
Yan Sun ◽  
Eric Pearlman
Keyword(s):  
Epithelial Cells ◽  
Interferon Γ ◽  
Cell Surface Expression ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Corneal Inflammation ◽  
Tyrosine Kinase 2 ◽  
Direct Binding ◽  
Ifn Γ

The inability of epithelial cells from the cornea and other tissues to respond to LPS is reportedly due to low expression of the TLR4 co-receptor MD-2. We generated MD-2−/− bone marrow chimeras, and showed that MD-2 expression on non-myeloid cells was sufficient to mediate LPS-induced corneal inflammation. As IFN-γ is produced during Pseudomonas aeruginosa corneal infection, we examined the role of this cytokine on MD-2 expression by primary human corneal epithelial (HCE) cells and HCE cell lines. Exogenous IFN-γ was found to induce MD-2 mRNA, MD-2 cell surface expression, and LPS responsiveness as determined by p65 translocation to the nucleus and production of IL-6, CXCL1, and CXCL8/IL-8. Incubation with either the AG490 JAK2 inhibitor or with STAT1 siRNA blocked STAT1 phosphorylation and MD-2 transcription. Furthermore, EMSA analysis demonstrated that STAT1 binds to the MD-2 promoter, indicating that STAT1 is an MD-2 transcription factor. Together, these findings demonstrate that IFN-γ induces MD-2 expression and LPS responsiveness in HCE cells by JAK-2-dependent STAT1 activation and direct binding to the MD-2 promoter. Furthermore, given our findings on LPS-induced corneal inflammation, it is likely that IFN-γ-induced MD-2 expression by corneal epithelial cells contributes to the host response in vivo, determining the extent of tissue damage and bacterial clearance.

Altered phenotype of cultured urothelial and other stratified epithelial cells: implications for wound healing

2006 ◽  
Vol 291 (1) ◽  
pp. F9-F21 ◽  
Author(s):  
Tung-Tien Sun
Keyword(s):  
Epithelial Cells ◽  
Wound Repair ◽  
Cultured Cells ◽  
Normal Epithelium ◽  
Corneal Epithelial Cells ◽  
Tissue Specific ◽  
Corneal Epithelial ◽  
Cultured Epithelial Cells ◽  
Normal Differentiation

The differentiation of cultured stratified epithelial cells can deviate significantly from that of normal epithelium, leading to suggestions that cultured cells undergo abnormal differentiation, or a truncated differentiation. Thus cultured epidermal and corneal epithelial cells stop synthesizing their tissue-specific keratin pair K1/K10 and K3/K12, respectively. The replacement of these keratins in the suprabasal compartment by K6/K16 keratins that are made by all stratified squamous epithelia during hyperplasia rules out a truncated differentiation. Importantly, the keratin pattern of in vivo corneal epithelium undergoing wound repair mimics that of cultured rabbit corneal epithelial cells. Although cultured urothelial cells continue to synthesize uroplakins, which normally form two-dimensional crystalline urothelial plaques covering almost the entire apical urothelial surface, these proteins do not assemble into crystals in cultured cells. Cultured epithelial cells can, however, rapidly regain normal differentiation on the removal of mitogenic stimuli, the use of a suitable extracellular matrix, or the transplantation of the cells to an in vivo, nonmitogenic environment. These data suggest that cultured epithelial cells adopt altered differentiation patterns mimicking in vivo regenerating or hyperplastic epithelia. Blocking the synthesis of tissue-specific differentiation products, such as the K1 and K10 keratins designed to form extensive disulfide cross-links in cornified cells, or the assembly of uroplakin plaques allows epithelial cells to better migrate and proliferate, activities that are of overriding importance during wound repair. Cultured urothelial and other stratified epithelial cells provide excellent models for studying the regulation of the synthesis and assembly of differentiation products, a key cellular process during epithelial wound repair.

scholarly journals Elovanoid-N32 or RvD6-isomer decrease ACE2 and binding of S protein RBD after injury or INFγ in the eye

2020 ◽  
Author(s):  
Thang L. Pham ◽  
Jiucheng He ◽  
Azucena H. Kakazu ◽  
Jorgelina Calandria ◽  
Khanh V. Do ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Lipid Mediators ◽  
Corneal Epithelial Cells ◽  
Health Crisis ◽  
S Protein ◽  
Corneal Epithelial ◽  
Angiotensin Converting Enzyme 2 ◽  
Virus Attachment ◽  
Human Corneal Epithelial Cells

Abstract The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection that causes coronavirus disease 2019 (COVID-19) has resulted in a pandemic affecting the most vulnerable in society, triggering a public health crisis and economic tall around the world. Effective treatments to mitigate this virus infection are needed. Since the eye is a route of virus entrance, we use an in vivo rat model of corneal inflammation as well as human corneal epithelial cells in culture challenged with IFNγ to study this issue. We explore ways to block the receptor-binding domain (RBD) of SARS-CoV-2 spike (S) protein to angiotensin-converting enzyme 2 (ACE2). Elovanoid (ELV)-N32 or Resolvin D6-isomer (RvD6i), among the lipid mediators studied, consistently decreased the expression of the ACE2 receptor, furin, and integrins in damaged corneas or IFNγ stimulated human corneal epithelial cells (HCEC). There was also a concomitant decrease in the binding of spike RBD with the lipid treatments. Concurrently, we uncovered that the lipid mediators also attenuated the expression of cytokines that participate in the cytokine storm, hyper-inflammation and senescence programming. Thus, the bioactivity of these lipid mediators will contribute to opening therapeutic avenues for COVID-19 by counteracting virus attachment and entrance to the eye and other cells and the ensuing disruptions of homeostasis.

scholarly journals In Vivo Confocal Microscopic Observations of Vortex Keratopathy in Patients with Amiodarone-Induced Keratopathy and Fabry Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Yasuhito Ikegawa ◽  
Atsushi Shiraishi ◽  
Yasuhito Hayashi ◽  
Akiyoshi Ogimoto ◽  
Yuichi Ohashi
Keyword(s):  
Epithelial Cells ◽  
Fabry Disease ◽  
Tear Film ◽  
Amiodarone Therapy ◽  
Slit Lamp ◽  
Epithelial Stem Cells ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial ◽  
Slit Lamp Biomicroscopy

Purpose. To compare the morphology of two types of vortex keratopathy: amiodarone-induced keratopathy and the Fabry disease-associated keratopathy. Patients and Methods. Eight patients who were receiving oral amiodarone therapy and 3 patients with Fabry disease, a mother and her 2 daughters, were examined by slit-lamp biomicroscopy and in vivo confocal microscopy (IVCM) regularly. Results. Amiodarone-induced keratopathy developed in 7 of the 8 patients, and it was detected as early as 7 days by IVCM and 14 days by slit-lamp biomicroscopy. The in vivo confocal microscopic images showed a clustering of corneal epithelial cells with a highly reflective cytoplasm in both types of keratopathy. In the amiodarone-induced keratopathy, the highly reflective epithelial cells were first found at the center of the cornea and then spread to the periphery with increasing time on amiodarone. In Fabry disease, the highly reflective epithelial cells were consistently observed extending from the limbus to the central cornea. Conclusion. These findings suggest that the corneal epithelial cells most likely endocytose amiodarone from the tear film in the amiodarone-induced keratopathy. In Fabry disease, globotriaosylceramide deposits are taken up by the lysosomes of the limbal epithelial stem cells, and they differentiate and migrate to the center of the cornea to form the whorl pattern.

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