Chan-Ling T, Stone J
Department of Anatomy, University of Sydney, Australia.
Invest Ophthalmol Vis Sci. 1992 Jun;33(7):2148-59.
This study addresses the role of astrocytes in the genesis of retinopathy of prematurity, examined in the feline model of this condition. Evidence is presented that the hypoxia of retinopathy of prematurity, in addition to inducing vasoproliferation, damages the retina directly. Retinal neurons survive the hypoxia, but the astrocytes, which are involved in the formation of the glia limitans of the retinal vessels, degenerate. Astrocytes subsequently recolonize the retina after a delay that matches the period of leakiness of the proliferative vasculature (described in the companion article). Given the evidence from other studies that the barrier properties of vessels are induced by their glia limitans, the authors suggest that the initial lack of barrier properties in the new vasculature is caused by the degeneration of astrocytes and that the subsequent formation of those properties is induced by the astrocytes that recolonize the retina some days later. The observation that astrocytes are more sensitive to hypoxia than neurons, at least in developing tissue, was unexpected. The literature reporting on the damage caused to central nervous tissue by hypoxia is consistent in assessing neurons as more sensitive and glial changes as a reaction to neuronal damage. The sensitivity of astrocytes found in this study and earlier in vitro research suggests that degenerated astrocytes can be replaced and their structural and functional relationships reestablished.
本研究探讨了星形胶质细胞在早产儿视网膜病变发生过程中的作用，该研究在这种疾病的猫模型中进行。有证据表明，早产儿视网膜病变的缺氧除了诱导血管增殖外，还直接损害视网膜。视网膜神经元在缺氧状态下存活，但参与视网膜血管胶质界膜形成的星形胶质细胞会退化。星形胶质细胞随后会在一段时间后重新定殖于视网膜，这段延迟时间与增殖性血管系统渗漏的时期相匹配（在配套文章中有所描述）。鉴于其他研究表明血管的屏障特性是由其胶质界膜诱导产生的，作者认为新血管系统最初缺乏屏障特性是由星形胶质细胞的退化所致，而这些特性随后的形成是由数天后重新定殖于视网膜的星形胶质细胞诱导产生的。至少在发育中的组织中，星形胶质细胞对缺氧比神经元更敏感这一观察结果出乎意料。关于缺氧对中枢神经组织造成损害的文献报道一致认为神经元更敏感，而胶质细胞的变化是对神经元损伤的一种反应。本研究以及早期体外研究中发现的星形胶质细胞的敏感性表明，退化的星形胶质细胞可以被替代，其结构和功能关系可以重新建立。
