scholarly journals Extracellular Vesicles Secreted by Corneal Epithelial Cells Promote Myofibroblast Differentiation

Cells ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 1080 ◽  
Author(s):  
Tina B. McKay ◽  
Audrey E. K. Hutcheon ◽  
James D. Zieske ◽  
Joseph B. Ciolino
Keyword(s):  
Epithelial Cells ◽  
Extracellular Vesicles ◽  
Corneal Epithelium ◽  
Smooth Muscle Actin ◽  
Initial Response ◽  
Protein Translation ◽  
Myofibroblast Differentiation ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial

The corneal epithelium mediates the initial response to injury of the ocular surface and secretes a number of profibrotic factors that promote corneal scar development within the stroma. Previous studies have shown that corneal epithelial cells also secrete small extracellular vesicles (EVs) in response to corneal wounding. In this paper, we hypothesized that EVs released from corneal epithelial cells in vitro contain protein cargo that promotes myofibroblast differentiation, the key cell responsible for scar development. We focused on the interplay between corneal epithelial-derived EVs and the stroma to determine if the corneal fibroblast phenotype, contraction, proliferation, or migration were promoted following vesicle uptake by corneal fibroblasts. Our results showed an increase in myofibroblast differentiation based on α-smooth muscle actin expression and elevated contractility following EV treatment compared to controls. Furthermore, we characterized the contents of epithelial cell-derived EVs using proteomic analysis and identified the presence of provisional matrix proteins, fibronectin and thrombospondin-1, as the dominant encapsulated protein cargo secreted by corneal epithelial cells in vitro. Proteins associated with the regulation of protein translation were also abundant in EVs. This paper reveals a novel role and function of EVs secreted by the corneal epithelium that may contribute to corneal scarring.

Recombinant TIMP-1 and -2 enhance the proliferation of rabbit corneal epithelial cells in vitro and the spreading of rabbit corneal epithelium in situ

1998 ◽  
Vol 17 (1) ◽  
pp. 47-52 ◽  
Author(s):  
Shizuya Saika ◽  
Yoshiji Kawashima ◽  
Yuka Okada ◽  
Sai-Ichi Tanaka ◽  
Osamu Yamanaka ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Corneal Epithelium ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial

scholarly journals Mannose Induces the Release of Cytopathic Factors from Acanthamoeba castellanii

1998 ◽  
Vol 66 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Henry Leher ◽  
Robert Silvany ◽  
Hassan Alizadeh ◽  
Jing Huang ◽  
Jerry Y. Niederkorn
Keyword(s):  
Epithelial Cells ◽  
Corneal Epithelium ◽  
Antimicrobial Agents ◽  
Chinese Hamster ◽  
Acanthamoeba Castellanii ◽  
Chronic Inflammatory Disease ◽  
Phenylmethylsulfonyl Fluoride ◽  
Corneal Epithelial Cells ◽  
Corneal Epithelial

ABSTRACT Acanthamoeba keratitis is a chronic inflammatory disease of the cornea which is highly resistant to many antimicrobial agents. The pathogenic mechanisms of this disease are poorly understood. However, it is believed that the initial phases in the pathogenesis of Acanthamoeba keratitis involve parasite binding and lysis of the corneal epithelium. These processes were examined in vitro, usingAcanthamoeba castellanii trophozoites. Parasites readily adhered to Chinese hamster corneal epithelial cells in vitro; however, parasite binding was strongly inhibited by mannose but not by lactose. Although mannose prevented trophozoite binding, it did not affect cytolysis of corneal epithelial cells. Moreover, mannose treatment induced trophozoites to release cytolytic factors that lysed corneal epithelial cells in vitro. These factors were uniquely induced by mannose because supernatants collected from either untreated trophozoites or trophozoites treated with other sugars failed to lyse corneal cells. The soluble factors were size fractionated in centrifugal concentrators and found to be ≥100 kDa. Treatment of the supernatants with the serine protease inhibitor phenylmethylsulfonyl fluoride inhibited most, but not all, of the cytopathic activity. These data suggest that the binding ofAcanthamoeba to mannosylated proteins on the corneal epithelium may exacerbate the pathogenic cascade by initiating the release of cytolytic factors.

In Vitro Toxicity of Netilmicin and Ofloxacin on Corneal Epithelial Cells

Cornea ◽  
2003 ◽  
Vol 22 (5) ◽  
pp. 468-472 ◽  
Author(s):  
Anna Claudia Scuderi ◽  
Grazia Maria Paladino ◽  
Clara Marino ◽  
Francesco Trombetta
Keyword(s):  
Epithelial Cells ◽  
In Vitro Toxicity ◽  
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.

Cornea and Lens Problems in Aniridia

2010 ◽  
Author(s):  
Edward J. Holland ◽  
Mayank Gupta
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Corneal Epithelium ◽  
Basal Layer ◽  
Limbal Stem Cells ◽  
Corneal Epithelial Cells ◽  
Film Stability ◽  
Corneal Epithelial ◽  
Corneal Erosion ◽  
Peripheral Cornea

The corneal epithelium is a rapidly regenerating, stratified squamous epithelium. Homeostasis of corneal epithelial cells is an important prerequisite, not only for the integrity of the ocular surface, but also for the visual function. The maintenance of a healthy corneal epithelium under both normal and wound-healing conditions is achieved by a population of stem cells located in the basal layer of limbal epithelium. The Limbus represents the transition zone between the peripheral cornea and the bulbar conjunctiva. The stem cells from the limbus generate the transient amplifying cells that migrate, proliferate, and differentiate to replace lost or damaged corneal epithelial cells. In patients with aniridia, there is a primary dysfunction of these limbal stem cells (see Figure 6.1). The cornea is affected clinically in 90 percent of the patients with aniridia. In most cases, the cornea in aniridic patients appears normal and transparent during infancy and childhood. However, during the early teens, the cornea begins to show changes. The early changes are marked by the in-growth of opaque epithelium from the limbal region into the peripheral cornea, which represents conjunctival epithelial cells, goblet cells, and blood vessels in the corneal epithelium. These changes gradually progress toward the central cornea and may cause corneal epithelial erosions and epithelial abnormalities that eventually culminate in opacification of the corneal stroma, which leads to vision loss. With the gradual loss of limbal stem cells, the entire cornea becomes covered with conjunctival cells. Eventually, many patients develop total limbal stem cell deficiency. These abnormalities usually become more pronounced with aging. The corneal abnormalities seen in aniridia are collectively termed “aniridic keratopathy”. Significant corneal opacification may occasionally be the initial manifestation of aniridia. Abnormal tear film stability and meibomian gland dysfunction are also observed in patients with aniridia. This can lead to dry eyes, aggravating corneal erosion and ulceration observed in aniridic patients. Sometimes, aniridia is associated with “Peter’s anomaly,” in which central corneal opacity is present at birth along with defects in the corneal endothelium and Descemet’s membrane.

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