Riley G P, Harrall R L, Cawston T E, Hazleman B L, Mackie E J
Rheumatology Research Unit, Addenbrooke's Hospital, Cambridge, United Kingdom.
Am J Pathol. 1996 Sep;149(3):933-43.
We investigated the distribution of tenascin in supraspinatus tendons to determine whether an alteration in tenascin expression was associated with human tendon degeneration. Tenascin was present in all of the tendons studied, although with two distinct patterns of expression. First, tenascin was associated with organized, fibrous regions of the tendon matrix that were typical of the normal tendon structure. This distribution is consistent with a role for tenascin in collagen fibril organization, perhaps maintaining the interface between fibrils and adjacent structures. Second, although tenascin was generally absent from poorly organized matrix in degenerate tendons, it was strongly associated with some rounded cells in disorganized fibrocartilaginous regions that were more abundant in pathological specimens. Tenascin was also found around infiltrating blood vessels, with more intense staining associated with a mononuclear cell infiltrate. Western blotting of tendon extracts showed differences in tenascin isoform expression, with only the small (200-kd) tenascin isoform found in normal tendons. Degenerate tendons also expressed the 300-kd isoform, consistent with a role for the larger tenascin isoform in tendon disease, potentially stimulating tenocyte proliferation, cell rounding, and fibrocartilaginous change. Proteolytic fragments of tenascin were detected but only in ruptured tendons, an indication of matrix remodeling in degenerate tendons, with fragment sizes consistent with the activity of matrix metalloproteinase enzymes.
我们研究了腱生蛋白在冈上肌腱中的分布,以确定腱生蛋白表达的改变是否与人类肌腱退变有关。在所研究的所有肌腱中均存在腱生蛋白,不过其表达模式有两种不同类型。首先,腱生蛋白与肌腱基质中典型的正常肌腱结构的有组织的纤维区域相关。这种分布与腱生蛋白在胶原纤维组织中的作用一致,可能维持了纤维与相邻结构之间的界面。其次,虽然在退变肌腱中结构不良的基质中通常不存在腱生蛋白,但它与一些圆形细胞强烈相关,这些圆形细胞存在于结构紊乱的纤维软骨区域,在病理标本中更为丰富。在浸润血管周围也发现了腱生蛋白,单核细胞浸润处染色更强。肌腱提取物的蛋白质印迹分析显示腱生蛋白异构体表达存在差异,正常肌腱中仅发现小(200-kd)的腱生蛋白异构体。退变肌腱还表达300-kd异构体,这与较大的腱生蛋白异构体在肌腱疾病中的作用一致,可能刺激腱细胞增殖、细胞变圆和纤维软骨改变。检测到了腱生蛋白的蛋白水解片段,但仅在断裂的肌腱中检测到,这表明退变肌腱中存在基质重塑,片段大小与基质金属蛋白酶的活性一致。