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Q.C. Ngumah, R.R. Pfister, C.I. Sommers; Immunohistochemical Study of PKC and PKC– Expression During Wound Healing in Alkali versus Abrasion Models of Corneal Injuries . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2754.
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To investigate if there are changes in the expression of Protein Kinase C (PKC) and specifically PKC–α during wound healing in the epithelium of alkali–injured corneas. The levels of PKC and more specifically PKC–α appears to increase in abrasion–models of normal corneal wound healing. PKC–α is involved in a number of signaling pathways that regulate Integrins and activate Fibronectin and a number of other extracellular matrix (ECM) and cell surface adhesion molecules all of which are of particular significance during wound healing. Comparable studies have not been done in an alkali–injured model in which wound healing often does not resolve normally.
Sixty rabbits were randomly assigned to one of two groups. In Group 1 (n = 30), the central corneal area of one eye was exposed to 1N NaOH for 35 seconds resulting in an 11mm alkali burn. In Group 2 (n = 30), an 11mm area of the central corneal epithelium of one eye was trephined and abraded to simulate an abrasion injury. Contralateral eyes served as a control in both groups. From each group, 3 animals were sacrificed at 48, 72, 84, 96, and 114hrs. Corneal sections were examined by indirect immunofluorescence for changes in epithelial PKC and PKC–α. Corneal sections were compared from alkali (Group 1)and abrasion–injured (Group 2) eyes and from non–treated control eyes. Quantification was done by analysis of fluorescence intensities histograms.
Results show a peak increase in epithelial PKC (28.4%) and PKC–α (32%) during wound healing in abrasion–injured corneas. This however was not evident in the alkali–injured corneas. Both PKC and PKC–α levels were also significantly higher in abraded versus alkali–injured corneas at all time intervals. Also after an initial increase, PKC and PKC–α were markedly reduced at 84hrs in alkali–injured corneas (33% and 33.5% reduction respectively).
These results suggest that the loss of PKC and PKC– α seen in the alkali–injury model may play a significant role in the persistent epithelial defects associated with this form of corneal injury. This is even more striking since the marked loss of both PKC and PKC– α at 84 hrs coincides with the time of reversal of movement of the leading epithelial edge found previously by our laboratory.
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