Basement membranes are highly specialized extracellular matrices. More than providing scaffolds, basement membranes are recognized as dynamic and versatile structures that modulate cellular responses to regulate tissue development, function, and repair. Increasing evidence suggests that, in addition to providing structural support to adjacent cells, basement membranes serve as reservoirs and modulators of growth factors that direct and fine-tune cellular functions. Since the corneal stroma is avascular and has a relatively low keratocyte density, it's likely that the corneal BM is different in composition from the BMs in other tissues. BMs are composed of a diverse assemblage of extracellular molecules, some of which are likely specific to the tissue where they function; but in general they are composed of four primary components-collagens, laminins, heparan sulfate proteoglycans, and nidogens-in addition to other components such as thrombospondin-1, matrilin-2, and matrilin-4 and fibronectin. Severe injuries to the cornea, including infection, surgery, and trauma, may trigger the development of myofibroblasts and fibrosis in the normally transparent connective tissue stroma. Ultrastructural studies have demonstrated that defective epithelial basement membrane (EBM) regeneration after injury to the cornea underlies the development of myofibroblasts from both bone marrow- and keratocyte-derived precursor cells. Defective EBM permits epithelium-derived and tear-derived transforming growth factor beta (TGF-β), platelet-derived growth factor (PDGF), and possibly other modulators, to penetrate the stroma at sustained levels necessary to drive the development and persistence of vimentin + alpha-smooth muscle actin + desmin+ (V + A + D+) mature myofibroblasts. A recent discovery that has contributed to our understanding of haze development is that keratocytes and corneal fibroblasts produce critical EBM components, such as nidogen-1, nidogen-2 and perlecan, that are essential for complete regeneration of a normal EBM once laminin secreted by epithelial cells self-polymerizes into a nascent EBM. Mature myofibroblasts that become established in the anterior stroma are a barrier to keratocyte/corneal fibroblast contributions to the nascent EBM. These myofibroblasts, and the opacity they produce, often persist for months or years after the injury. Transparency is subsequently restored if the EBM is fully regenerated, myofibroblasts are deprived of TGF-β and undergo apoptosis, and keratocytes reoccupy the anterior stroma and reabsorb the disordered extracellular matrix.

中文翻译：

---

角膜上皮基底膜：结构，功能和再生。

基底膜是高度专业化的细胞外基质。基底膜不只是提供支架，还被认为是动态的多功能结构，可调节细胞反应以调节组织的发育，功能和修复。越来越多的证据表明，除了为相邻细胞提供结构支持外，基底膜还可以充当指导和微调细胞功能的生长因子的储存库和调节剂。由于角膜基质是无血管的，并且角膜细胞密度相对较低，因此，角膜BM的成分可能与其他组织的BM不同。BM由多种不同的细胞外分子组成，其中一些可能对它们起作用的组织具有特异性。但总体来说，它们是由四个主要组成部分组成的-Collagens，层粘连蛋白，硫酸乙酰肝素蛋白聚糖和尼古丁-以及其他成分，例如血小板反应蛋白1，matrilin-2和matrilin-4和纤连蛋白。对角膜的严重伤害，包括感染，手术和外伤，可能会触发通常透明的结缔组织基质中成肌纤维细胞的形成和纤维化。超微结构研究表明，角膜损伤后上皮基底膜（EBM）的缺陷再生是源自骨髓和角化细胞的前体细胞形成成肌纤维细胞的基础。缺陷性EBM允许上皮来源和眼泪来源的转化生长因子β（TGF-β），血小板衍生生长因子（PDGF）以及其他可能的调节剂，以持续的水平穿透基质，以驱动波形蛋白+α平滑肌肌动蛋白+结蛋白+（V + A + D +）成熟的成肌纤维细胞的发育和持久性。最近的发现有助于我们了解雾霾的发展，这是角膜细胞和角膜成纤维细胞产生关键的EBM成分，例如nidogen-1，nidogen-2和perlecan，一旦上皮层粘连蛋白分泌，它们对于正常EBM的完全再生是必不可少的。细胞自聚合成新生的EBM。在前间质中形成的成熟肌成纤维细胞是新生角膜基质细胞对角膜细胞/角膜成纤维细胞贡献的障碍。这些成肌纤维细胞及其产生的不透明性通常在受伤后持续数月或数年。如果完全重新生成了EBM，则可​​以恢复透明度。