Location and expression of galactose β-1,4-glycosidic bonds in keloid tissue / 中华皮肤科杂志

ABSTRACT

Objective To observe the expression and location of galactose β-1,4-glycosidic bonds (Gal β-1,4-GlcNAc) in keloid tissue,and to investigate the role of glycoprotein galactosylation in the formation of keloid.Methods This study included 10 keloid tissue specimens,7 hyperplastic scar tissue specimens,and 6 normal skin specimens.Lectin blot analysis was performed to measure the glycosylation level of glycoproteins,saturated picric acid-Sirius red staining followed by polarization microscopy to observe the type,expression and distribution of collagens in these specimens.The type Ⅰ/type Ⅲ collagen ratio was calculated.Immunofluorescence-based histochemistry was carried out by using Ricinus communis agglutinin I to analyze the expression and location of Gal β-1,4-GlcNAc in these skin samples,and double immunofluorescent staining to observe the colocalization of Gal β-1,4-GlcNAc and type Ⅰ procollagen α1.Results Compared with the normal skin tissue,the keloid tissue showed a significant increase in the expression of Gal β-1,4-GlcNAc in glycoproteins with a relative molecular mass of 30 000 to 40 000.Polarization microscopy revealed that there was a considerable expression of type Ⅰ collagen fibers,which amounted to (71.53 ± 4.03)％ in all the collagen fibers.The type Ⅰ/type Ⅲ collagen ratio was significantly higher in keloid tissue specimens than in normal tissue specimens (2.56 ± 0.53 vs.0.91 ± 0.11,P ＜0.05).Fluorescence microscopy showed that Gal β-1,4-GlcNAc was uniformly distributed in the membrane and cytoplasm of fibroblasts in keloid tissue,and the expression intensity of Gal β-1,4-GlcNAc in keloid tissue was notably stronger than that in normal skin tissue.There was a colocalization between Gal β-1,4-GlcNAc and type Ⅰ procollagen α1 in keloid tissue.Conclusions The expression of Gal β-1,4-GlcNAc,which is mainly observed in fibroblasts,is upregulated in keloid tissue,suggesting that Gal β-1,4-GlcNAc may be involved in the modulation of factors responsible for excessive fibre formation during the repair process of keloid.