PerspectiveCorneal cells: chatty in development, homeostasis,wound healing, and disease☆
Section snippets
Cell communication in corneal development
The cornea develops from ectoderm giving rise to the epithelium and neural crest cells giving rise to keratocytes, endothelial cells, and nerve cells.1, 2, 3 Both neurogenic and nonneurogenic neural crest cells contribute to corneal development.4 Recent studies suggest that the lens-derived signals are important in directing the development of the neural crest-derived cells that contribute to the cornea.5
Cytokine- and growth factor–mediated communications are likely involved in directing neural
Cell communication in corneal homeostasis
Maintenance of normal corneal structure and function requires ongoing communication between corneal epithelial cells, keratocytes, and nerve cells. We previously hypothesized6 that maintenance of the Bowman layer requires ongoing cytokine–mediated stromal–epithelial interactions and that this layer is a visible sign of these incessant attractive and repulsive cellular communications (Figure 1).6 It seems likely that endothelial cells also communicate with keratocytes during homeostasis,
Cell communication after corneal injury
Stromal–epithelial communications lie at the heart of the corneal wound healing response to epithelial and stromal injury.9 Injuries may be related to trauma, infection, surgery, and other initiators. These initiators are typically associated with epithelial injury and resulting communication to keratocytes, kertoblasts, myofibroblasts, and inflammatory cells.
The earliest stromal event after epithelial injury is death of underlying keratocyte cells.16 Initially, regardless of the source of
Cell communication associated with corneal disease
Cytokine–mediated cellular communications between cells of the cornea are very complex. A thorough understanding of these interactions is a key to in depth appreciation of pathophysiology and possibly effective treatment for many corneal disorders and diseases. Some of these cellular interactions are only activated in response to disease. In other cases, inauspicious activation of the cellular communications appears to have a role in the pathophysiology of particular diseases. Acquired or
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2024, A Comprehensive Guide to Toxicology in Nonclinical Drug DevelopmentECM stiffness modulates the proliferation but not the motility of primary corneal keratocytes in response to PDGF-BB
2022, Experimental Eye ResearchCitation Excerpt :In the cornea, PDGF-BB is expressed within the corneal epithelium (Kim et al., 1999) and is also present in tear fluid (Tuominen et al., 2001; Vesaluoma et al., 2009). Following an injury, PDGF-BB is released into the stromal compartment and is thought to stimulate the migration and mitosis of corneal keratocytes (Kamil and Mohan, 2020; Kim et al., 2009; Wilson et al., 2003). Consistent with this idea, treatment with PDGF-BB has been shown to promote a more elongated keratocyte morphology in culture (Jester and Ho-Chang, 2003), as well as increases in both cell proliferation (Denk and Knorr, 1997; Kim et al., 1999) and motility (Andresen et al., 1997; Andresen and Ehlers, 1998; Kim et al., 2009).
Analysis of different conditioned media secreted by limbal progenitor cells in the modulation of corneal healing
2022, Experimental Eye ResearchBiological effects of mitomycin C on late corneal haze stromal fibrosis following PRK
2020, Experimental Eye ResearchMitomycin C modulates intracellular matrix metalloproteinase-9 expression and affects corneal fibroblast migration
2019, European Journal of Pharmacology
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This study was supported in part by EY10056 and EYO1730 from the National Eye Institute and by an Unrestricted Grant from Research to Prevent Blindness, New York, New York.