The role of novel extracellular matrix protein on CNS regeneration and its application study for glaucoma treatment

在我们利用FISH衍生分子进行哺乳动物视神经再生的策略中，我们通过腺相关病毒载体在大鼠视网膜中使用了紫蛋白(一种新的细胞外基质蛋白)过表达系统。在大鼠，补充紫红素可通过粘着斑激酶(FAK)/Akt活化机制保护视网膜神经节细胞(RGCs)免受损伤诱导的细胞凋亡。此外，紫红素涂层培养皿对大鼠视网膜神经节细胞具有黏附作用。我们重点研究了细胞外基质相关分子作为紫红素黏附和存活效应的机制。紫红素抑制视神经损伤诱导的基质金属蛋白酶9活性和层粘连蛋白的降解，并激活FAK信号。紫红素可能为开发青光眼等人类视网膜退行性疾病的治疗方法提供新的途径。

In our strategies toward optic nerve regeneration of mammals using fish derived molecule, we used purpurin(a novel extracellular matrix protein) overexpression systems by adeno-associated virus vector in rat retina. In rat, supply of purpurin could protect retinal ganglion cells(RGCs) from injury-induced apoptosis through a mechanism of focal adhesion kinase(FAK)/Akt activation. Furthermore, purpurin had adhesive effect on rat RGCs from culture study with purpurin-coated dishes. We focused on the extracellular matrix-related molecules as a mechanism of purpurin adhesive and survival effects. Purpurin inhibited optic injury-induced matrix metalloprotease 9 activity and the degradation of laminin and activated FAK signaling. Purpurin could potentially offer new avenues for developing treatments for human retinal degenerative disorders such as glaucoma.