Eye (London, England) · 1998
Tenascin-cytotactin (TN-C) variants in pseudophakic/aphakic bullous keratopathy corneas.
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Maseruka H, Ataullah S M, Zardi L, Tullo A B, Ridgway A E, Bonshek R E
Аннотация
PURPOSE: To examine pseudophakic/aphakic bullous keratopathy (PBK/ABK) human corneas for patterns of expression of tenascincytotactin (TN-C) variants known to mediate specific cellular functions, viz. anti-adhesion (high molecular mass (M(r))) and adhesion (low/intermediate M(r)).
METHODS: PBK/ABK corneas were selected to encompass only those with bullae and without inflammation, scarring or neovascularisation. Serial sections from these and normal corneas were labelled with antibodies BC-4 (recognising all TN-C variants) and BC-2 (specific for the high M(r) TN-C variant). Bound antibody was revealed with an avidin-biotin peroxidase technique. In a given pair of corneal sections, positivity with BC-4 but not BC-2 indicates localisation of low/ intermediate M(r) TN-C variants and absence of the high M(r) TN-C variant. BC-2 identifies the high M(r) variant.
RESULTS: There was no immunostaining with either BC-2 or BC-4 in normal corneas except at the corneoscleral interface, where both BC-2 and BC-4 were immunolocalised. In PBK/ABK corneas, BC-2 staining was seen in 5 of 13 corneas and was restricted mainly to epithelial basement membrane (BM) overlying bullae. BC-2 did not label the stroma. BC-4 immunostaining was present in all PBK/ABK corneas and was localised in epithelial BM, both epithelial and stromal borders of bullae, pannus, endothelial BM and in oedematous stromal regions.
CONCLUSIONS: TN-C variants are differentially expressed in PBK/ABK corneas. The high M(r) variant is restricted mainly to epithelial BM overlying bullae, while low/intermediate M(r) variants occur in epithelial BM, both epithelial and stromal borders of bullae, and in pannus. Given the in vitro functions of TN-C, a role for promoting epithelial dehiscence and reattachment to the substratum in PBK/ABK corneas by high and low/intermediate M(r) variants respectively is likely.
METHODS: PBK/ABK corneas were selected to encompass only those with bullae and without inflammation, scarring or neovascularisation. Serial sections from these and normal corneas were labelled with antibodies BC-4 (recognising all TN-C variants) and BC-2 (specific for the high M(r) TN-C variant). Bound antibody was revealed with an avidin-biotin peroxidase technique. In a given pair of corneal sections, positivity with BC-4 but not BC-2 indicates localisation of low/ intermediate M(r) TN-C variants and absence of the high M(r) TN-C variant. BC-2 identifies the high M(r) variant.
RESULTS: There was no immunostaining with either BC-2 or BC-4 in normal corneas except at the corneoscleral interface, where both BC-2 and BC-4 were immunolocalised. In PBK/ABK corneas, BC-2 staining was seen in 5 of 13 corneas and was restricted mainly to epithelial basement membrane (BM) overlying bullae. BC-2 did not label the stroma. BC-4 immunostaining was present in all PBK/ABK corneas and was localised in epithelial BM, both epithelial and stromal borders of bullae, pannus, endothelial BM and in oedematous stromal regions.
CONCLUSIONS: TN-C variants are differentially expressed in PBK/ABK corneas. The high M(r) variant is restricted mainly to epithelial BM overlying bullae, while low/intermediate M(r) variants occur in epithelial BM, both epithelial and stromal borders of bullae, and in pannus. Given the in vitro functions of TN-C, a role for promoting epithelial dehiscence and reattachment to the substratum in PBK/ABK corneas by high and low/intermediate M(r) variants respectively is likely.