TN—C与MDA-7在增生性瘢痕中表达与调控

增生性瘢痕是以皮肤损伤后成纤维细胞过度增殖为特征的一种病理改变，其发病机制尚不明确，目前没有有效的治疗方法。当皮肤组织损伤时，腱糖蛋白C（Tenascin-C，TN-C）具有多种不同的作用介导炎症和纤维化进程，并使组织有效修复。TN—C是细胞外基质中一个具有独特的六聚体结构的寡聚糖蛋白家族，TN—C一过性表达在器官形成期，在大多数成人组织不表达或表达极少。然而，在病理条件下TN—C表达增加，诸如炎症，伤口愈合和纤维化。TN—C参与胚胎形成、肿瘤发生及损伤修复过程有关，参与细胞黏附、增殖、迁徙、分化、细胞间相互作用以及细胞凋亡。黑色素瘤分化相关基因7／白介素24（MDA-7／IL-24）能选择性抑制瘢痕疙瘩中成纤维细胞的增殖，并诱导瘢痕疙瘩中成纤维细胞的凋亡，而对正常细胞无任何作用。MDA-7／IL-24很可能与瘢痕的形成有关。

The Expression and Regulation of TN-C andMDA-7 in Hypertrophic Scars

Hyperplastic scar are fibroproliferative dermal lesions characterized by the proliferation of fibroblasts and the pathogenesis is not clear, for which no effective treatment exists. Upon skin tissue damage, Tenascin-c plays a multitude of different roles that mediate both inflammatory and fibrotic processes to enable effective tissue repair. Tenascin-C （TN-C） is a huge extracellular matrix proteinthat consisting of 6 identical subunits constructed from a number of repeated domains. TN-C is expressed transiently during organogenesis and is absent or greatly reduced in most adult tissues. However, it increases again in pathological conditions such as inflammation, wound healing, and fibrosis. TN-C expression is often associated with formation of the embryo, tumorigenesis and damage repair, TN-C participates in a ina series of regulatory mechanisms involved in cell adhesion, proliferation activity, migration, differentiation, interaction and cell apoptosis.The studies showed that the exogenous IL-24gene could selectively inhibit human keloid fibroblasts proliferation and induce significant apoptosis, but no harmful effect was observed in normal cells. It is reported that IL-24 gene might be involved in the formation ofkeloids.