蛋白糖基化抑制剂对病理性瘢痕成纤维细胞Fas蛋白的表达与功能的影响

目的 研究N-糖链合成抑制剂衣霉素对病理性瘢痕成纤维细胞Fas蛋白的表达与诱导凋亡功能的影响.方法 瘢痕疙瘩及增生性瘢痕各5例,以健康皮肤为对照,免疫组织化学法检测组织中成纤维细胞Fas蛋白表达;组织块贴壁法培养成纤维细胞;Western Blot法及流式细胞术检测衣霉素处理及未处理各组成纤维细胞Fas蛋白水平的表达及凋亡率的变化.结果 病理性瘢痕及健康皮肤成纤维细胞胞质及胞膜中均可见Fas蛋白表达;增生性瘢痕、瘢痕疙瘩及健康皮肤成纤维细胞Fas蛋白糖基化水平依次降低,3组成纤维细胞在Fas单克隆抗体(Fas monoelonal antibody,FasMcAb)作用后凋亡率与Fas蛋白糖基化成正相关,衣霉素可明显降低病理性瘢痕成纤维细胞Fas蛋白糖基化水平,但对健康皮肤成纤维细胞Fas蛋白糖基化水平抑制作用不明显.结论 FasMcAb诱导病理性瘢痕成纤维细胞凋亡与成纤维细胞Fas蛋白糖基化水平成正相关,而衣霉素可显著降低成纤维细胞Fas蛋白糖基化水平.

The effect of tunicamycin on Fas protein expression and its function in fibroblasts from hypertrophic sear and keloid

Objective To detect the effect of tanicamycin on Fas protein expression and Fas monoclanal antibedy(FasMcAb)-induced apoptosis of fibroblast from hypertrophic scar and keloid. Methods The expression of Fas protein was detected by immunostaining in 5 cases of keloid, 5 cases of hypertrophic scar and 5 cases of normal skin as control. The fibroblasts were cultured and treated with tunieamycin. The Fas protein expression and the fibroblast apoptosis rate were assessed by Western Blot and flow cytometry. Results It revealed that Fas protein was detectable in all the three groups. The Fas glycosylation level was highest in hypertrophic scar, but lowest in normal skin. The FasMcAb-induced apoptosis had a positive relationship with the Fas glycosylation. Tunicamycin had a significant inhibitory effect on the Fas glycosylation in keloid and hypertrophic scar, but not in normal skin. Conclusions The FasMcAb-induced apoptosis has a positive relationship with the Fas glycosylation. Tunicamycin has a significant inhibitory effect on the Fas glycosylation inkeloid and hypertrophic scar.