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Corneal Wound Healing (corneal + wound_healing)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

4135: Matrix metalloproteinase 14 overexpression reduces corneal scarring

ACTA OPHTHALMOLOGICA, Issue 2010
S GALIACY
Purpose Corneal wound healing is an everyday preoccupation for ophthalmologists.Corneal transparency depends on the scarring quality after a traumatic corneal wound, but also after refractive corneal surgery. Cicatrisation and fibrosis formation involve epithelial/fibroblast interactions via paracrin signals inducing extracellular matrix (ECM) remodelling. The major event is fibroblast activation and differentiation into myofibroblasts. These cells have a key role in the fibrotic response. They acquire contractile properties, and synthetise a new ECM, mainly composed of type III collagen. This scar tissue is less organised than the regular stroma, thus explaining corneal opacity. ECM remodelling is a critical step which aims to digest the excess of ECM by proteolysis of type III collagen. MMP14 is a membrane-bound fibrillar collagenase from the Matrix Metalloprotease family. We hypothesised that its overexpression in the corneal stroma during wound repair will increase ECM remodelling and thus prevent collagen deposition in the scar tissue. Methods We developed an adeno-associated virus-based vector expressing murine MMP14 under the control of the CMV promoter. We evaluated MMP14 overexpression after viral transfection in a murine model of corneal wound healing. We characterised several parameters: clinical observation, histology, and wound healing markers. Results Our preliminary results showed a decreased in oedema and corneal scar formation, associated with a decreased expression of alpha smooth actin and type III collagen. Conclusion These results represent proof of concept that gene transfer of MMP14 can reduce scar formation, which could have therapeutic applications after corneal trauma. [source]

Trefoil factor 3 is induced during degenerative and inflammatory joint disease, activates matrix metalloproteinases, and enhances apoptosis of articular cartilage chondrocytes

ARTHRITIS & RHEUMATISM, Issue 3 2010
Sophie Rösler
Objective Trefoil factor 3 (TFF3, also known as intestinal trefoil factor) is a member of a family of protease-resistant peptides containing a highly conserved motif with 6 cysteine residues. Recent studies have shown that TFF3 is expressed in injured cornea, where it plays a role in corneal wound healing, but not in healthy cornea. Since cartilage and cornea have similar matrix properties, we undertook the present study to investigate whether TFF3 could induce anabolic functions in diseased articular cartilage. Methods We used reverse transcriptase,polymerase chain reaction, Western blot analysis, and immunohistochemistry to measure the expression of TFF3 in healthy articular cartilage, osteoarthritis (OA),affected articular cartilage, and septic arthritis,affected articular cartilage and to assess the effects of cytokines, bacterial products, and bacterial supernatants on TFF3 production. The effects of TFF3 on matrix metalloproteinase (MMP) production were measured by enzyme-linked immunosorbent assay, and effects on chondrocyte apoptosis were studied by caspase assay and annexin V assay. Results Trefoil factors were not expressed in healthy human articular cartilage, but expression of TFF3 was highly up-regulated in the cartilage of patients with OA. These findings were confirmed in animal models of OA and septic arthritis, as well as in tumor necrosis factor ,, and interleukin-1,,treated primary human articular chondrocytes, revealing induction of Tff3/TFF3 under inflammatory conditions. Application of the recombinant TFF3 protein to cultured chondrocytes resulted in increased production of cartilage-degrading MMPs and increased chondrocyte apoptosis. Conclusion In this study using articular cartilage as a model, we demonstrated that TFF3 supports catabolic functions in diseased articular cartilage. These findings widen our knowledge of the functional spectrum of TFF peptides and demonstrate that TFF3 is a multifunctional trefoil factor with the ability to link inflammation with tissue remodeling processes in articular cartilage. Moreover, our data suggest that TFF3 is a factor in the pathogenesis of OA and septic arthritis. [source]

4135: Matrix metalloproteinase 14 overexpression reduces corneal scarring

Keratocyte repopulation in UVB-exposed thioltransferase knockout mice

ACTA OPHTHALMOLOGICA, Issue 2007
A PODSKOCHY
Purpose: Thioltransferase is involved in cell protein homeostasis and DNA synthesis. It inhibits apoptosis and stimulates cell proliferation. Keratocyte repopulation after ultraviolet B (UVB) damage was studied in corneas of thioltransferase (-/-) mice. Methods: Six wild type mice and six thioltransferase (-/-) mice corneas were exposed at 300 nm UV-radiation at a dose producing damage in the corneal stroma (8 kJ/m2). Animals were killed 3 and 7 days after exposure. Corneas were processed for light microscopy. Results: All corneas of wild type mice and thioltransferase (-/-) mice showed extensive damage 3 days after UVB exposure. Keratocytes disappeared throughout the entire thickness of the UVB-damaged central stroma. Corneal thickness was nearly doubled compared with non-treated control corneas. However, 7 days after UVB exposure corneas of wild type mice were almost completely repopulated by keratocytes, only superficial ¼ of the stroma was still free of keratocytes. Corneal thickness was almost normal. Corneal stroma in the thioltransferase (-/-) mice 7 days after UV exposure was still not repopulated by keratocytes and the corneas were still very thick. Conclusions: The keratocyte repopulation in thioltransferase (-/-) mice is delayed. Thioltransferase seems to play an important role in the corneal wound healing and keratocyte repopulation after UVB induced damage. [source]

Expression of the focal adhesion protein PINCH in normal and alkali-injured corneas and the role of PMNs

ACTA OPHTHALMOLOGICA, Issue 4 2007
Beatrice Bourghardt Peebo
Abstract. Purpose:, To evaluate the role of particularly interesting new cysteine-histidine-rich protein (PINCH) in corneal wound healing and early neovascularization and to assess the influence of granulocytes. Methods:, A standardized corneal alkali wound was inflicted under general anaesthesia to the right eye of 14 New Zealand White rabbits. Seven of the rabbits received i.v. 5 mg/kg fucoidin every 2 hours to prevent granulocytes from entering the wound area. After 36 hours, the rabbits were killed, the corneas excised, fixed in 4% formaldehyde and embedded in paraffin. The sections were double-stained with antibodies against PINCH and with haematoxylin. Results:, In the normal cornea and limbus, PINCH was weakly expressed in the corneal epithelium and in a wedge of the conjunctival stroma. In the wounded corneas, PINCH expression was seen in the frontline of repopulating endothelial and epithelial cells, and in active keratocytes. The vascular endothelium and the granulocytes expressed PINCH, as did the conjunctival epithelium. In the fucoidin-treated rabbits, PINCH expression was markedly reduced. The vascular endothelial cells and the few granulocytes did not express PINCH in these rabbits. Conclusions:, PINCH is only slightly expressed in the normal cornea. A corneal wound induces PINCH expression in the repopulating cells, in the vascular endothelial cells of the limbus, in the limbal epithelium and in the granulocytes. Exclusion of granulocytes reduces expression of PINCH and there is no expression at all in the vascular endothelium. [source]