Keratocyte and fibroblast phenotypes in the repairing cornea

Me, Fini

doi:10.1016/s1350-9462(98)00033-0

Cited by 377 publications

(313 citation statements)

References 65 publications

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“…Following their migration, embryonic keratocytes begin to synthesize and secrete extracellular matrix components consisting of collagens types I, V, VI (Fini, 1999;Linsenmayer et al, 1983), as well as keratan sulfate, which exhibits a unique tissue-specific form of glycosylation in the cornea (Funderburgh, Mann, & Funderburgh, 2003). Between birth and eyelid opening, the number of proliferating keratocytes in the developing corneal stroma decreases dramatically from 20% of the total to nearly zero (Zieske, 2004).…”

Section: Keratocyte Origin and Plasticitymentioning

confidence: 99%

The keratocyte: Corneal stromal cell with variable repair phenotypes

West‐Mays

Dwivedi

2006

The International Journal of Biochemistry & Cell Biology

320

223

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Keratocytes, also known as fibroblasts, are mesencyhmal-derived cells of the corneal stroma. These cells are normally quiescent, but they can readily respond and transition into repair phenotypes following injury. Cytokines and other growth factors that provide autocrine signals for stimulating wound responses in resident cells are typically presented by platelets at the site of an injury. However, due to the avascular nature of the cornea many of the environmental cues are derived from the overlying epithelium. Corneal epithelial-keratocyte cell interactions have thus been extensively studied in numerous in vivo corneal wound healing settings, as well as in in vitro culture models. Exposure to the different epithelial-derived factors, as well as the integrity of the epithelial substratum, are factors known to impact the keratocyte response and determine whether corneal repair will be regenerative or fibrotic in nature. Finally, the recent identification of bone-marrow derived stem cells in the corneal stroma suggests a further complexity in the regulation of the keratocyte phenotype following injury. KeywordsKeratocyte; Cornea; Injury; Apoptosis; Myofibroblasts; Transparency; Plasticity Cell facts• Keratocytes are neural-crest derived mesenchymal cells that sparsely populate the corneal stroma.• Keratocytes are quiescent, dendritic cells that upon injury to the cornea are stimulated to either undergo apoptosis or transition into repair phenotypes.• Structural integrity of the basement membrane is critical for minimizing the fibrotic response of keratocytes and subsequent scarring and loss of corneal clarity.• Bone-marrow derived stem cells have been detected in the corneal stroma and may participate in the activation of the keratocytes following injury.

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Section: Keratocyte Origin and Plasticitymentioning

confidence: 99%

The keratocyte: Corneal stromal cell with variable repair phenotypes

West‐Mays

Dwivedi

2006

The International Journal of Biochemistry & Cell Biology

320

223

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“…The matrices undergo constant, slow remodelling during health and rapid remodelling during repair. [28][29][30][31][32] Corneal stromal remodelling during wound healing is mediated by a group of zinc containing degradative enzymes known as matrix metalloproteinases (MMPs). 33,34 They appear in a precisely controlled sequence that suggest they perform specific roles.…”

Section: Role Of Mmp Activitymentioning

confidence: 99%

Pathogenesis, clinical features and management of recurrent corneal erosions

Ramamurthi

Rahman

Dutton

et al. 2005

Eye

113

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Recurrent corneal erosions (RCE) are common. They are characterised by repeated episodes of pain, difficulty in opening the eyes, watering, and photophobia resulting from poor epithelial adhesion. In the majority of patients with RCE, trauma is the initiating factor. Epithelial, stromal, and endothelial corneal dystrophies have all been described in association with RCE. Other causes that may lead to RCE include chemical and thermal injuries, previous herpetic keratitis, meibomian gland dysfunction, ocular rosacea, diabetes mellitus, Salzmann's nodular degeneration, band keratopathy, previous bacterial ulceration, kerato-conjunctivitis sicca, and epidermolysis bullosa. The conditions that are associated with RCE can be either primary or secondary depending on whether the basement membrane complex abnormality is intrinsic or acquired. Primary types tend to be bilateral, symmetrical and develop in multiple corneal locations. The pathogenetic mechanism of this disorder is related to poor adhesion of the corneal epithelium to the underlying stroma. Excessive matrix metalloproteinase (MMP) activity may play a role in the pathogenesis. Although the majority of patients will respond to simple measures such as padding and antibiotic ointment, RCE resistant to simple measures require approaches that are more elaborate. The common goal of these approaches is to encourage proper formation of adhesion complexes between the epithelium and the stroma. The use of longterm contact lenses, autologous serum eye drops, botulinum toxin, induced ptosis, oral MMP inhibitors, diamond burr polishing of Bowman's membrane have been reported with varying degree of success in treating RCE. Anterior stromal puncture with insulin needles or Neodymium : aluminium-yttriumgarnet may enhance the epithelial adhesion to the basement membrane by scar formation and success rates of up to 80% have been reported in the treatment of recalcitrant RCE. Excimer laser photo-therapeutic keratectomy (PTK) is now a well-established treatment modality for RCE and is being used both safely and effectively. Partial ablation of Bowman's layer with PTK gives a smooth surface for the newly generating epithelium to migrate and form adhesion complexes. The pathogenesis, clinical features, and management options of this common disorder are discussed in this review article.

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“…Newly assembled immature collagen fibrils assemble, grow, and mature during postnatal development of the cornea (Birk et al, 1996;Birk, 2001). The corneal keratocyte is the major cell type in the corneal stroma that synthesizes the stromal extracellular matrix (Hamilton, 1972;Beales et al, 1999;Fini, 1999;Chakravarti et al, 2004). It secretes two fibril-forming collagens.…”

Section: Introductionmentioning

confidence: 99%

Collagen fibril assembly during postnatal development and dysfunctional regulation in the lumican‐deficient murine cornea

Chakravarti

Zhang

Chervoneva

et al. 2006

Developmental Dynamics

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The transparent cornea is the outer barrier of the eye and is its major refractive surface. Development of a functional cornea requires a postnatal maturation phase involving development, growth and organization of the stromal extracellular matrix. Lumican, a leucine-rich proteoglycan, is implicated in regulating assembly of collagen fibrils and the highly organized extracellular matrix essential for corneal transparency. We investigated the regulatory role(s) of lumican in fibril assembly during postnatal corneal development using wild type (Lum ϩ/ϩ ) and lumican-null (Lum Ϫ/Ϫ ) mice. In Lum ϩ/ϩ mice, a regular architecture of small-diameter fibrils is achieved in the anterior stroma by postnatal day 10 (P10), while the posterior stroma takes longer to reach this developmental maturity. Thus, the anterior and the posterior stroma follow distinct developmental timelines and may be under different regulatory mechanisms. In Lum Ϫ/Ϫ mice, it is the posterior stroma where abnormal lateral associations of fibrils and thicker fibrils with irregular contours are evident as early as P10. In contrast, the anterior stroma is minimally perturbed by the absence of lumican. In Lum ϩ/ϩ mice, lumican is expressed throughout the developing stroma at P10, with strong expression limited to the posterior stroma in the adult. Therefore, the posterior stroma, which is most vulnerable to lumican-deficiency, demonstrates an early developmental defect in fibril structure and architecture in the Lum Ϫ/Ϫ mouse. These defects underlie the reported increased light scattering and opacity detectable in the adult. Our findings emphasize the early regulation of collagen structure by lumican during postnatal development of the cornea. Developmental Dynamics 235:2493-2506, 2006.

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Keratocyte and fibroblast phenotypes in the repairing cornea

Cited by 377 publications

References 65 publications

The keratocyte: Corneal stromal cell with variable repair phenotypes

The keratocyte: Corneal stromal cell with variable repair phenotypes

Pathogenesis, clinical features and management of recurrent corneal erosions

Collagen fibril assembly during postnatal development and dysfunctional regulation in the lumican‐deficient murine cornea

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