Insulin‐related growth factors stimulate proliferation of retinal progenitors in the goldfish
Insulin‐related growth factors stimulate proliferation of retinal progenitors in the goldfish
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DOI：
10.1002/(sici)1096-9861(19980511)394:3
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发表时间：
1998-05
影响因子：
2.5
通讯作者：
Shayne E. Boucher;P. Hitchcock
中科院分区：
文献类型：
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作者：
Shayne E. Boucher;P. Hitchcock
成年金鱼的视网膜在动物的一生中不断生长，部分原因是新神经元的不断增加。此外，破坏该组织中现存的神经元刺激神经元再生。为了鉴定调节正常和损伤刺激的神经发生的生长因子，我们使用器官培养技术并测试了9种肽生长因子调节正常视网膜和病变视网膜中细胞增殖的能力。在测试的生长因子中，只有胰岛素相关肽（胰岛素和胰岛素样生长因子I和II）持续刺激增殖，并且这仅限于周向生发区内的视网膜祖细胞。测试的生长因子均不刺激视杆前体细胞（成熟视网膜中的细胞，其后代仅是视杆光感受器）或损伤刺激的视网膜祖细胞的增殖。尽管负面数据受到多种解释，但这些数据表明，在成年金鱼的视网膜中，胰岛素相关肽调节周围生发带内视网膜祖细胞的增殖，但调节成年金鱼视网膜中视杆前体细胞或损伤诱导的视网膜祖细胞增殖的分子尚未确定。神经学比较杂志394：386-394，1998.© 1998 Wiley利斯公司
The retina of the adult goldfish grows throughout the life of the animal, in part, by the continual addition of new neurons. Further, destruction of extant neurons in this tissue stimulates neuronal regeneration. In an attempt to identify growth factors that regulate both normal and injury‐stimulated neurogenesis, we used organ culture techniques and tested nine peptide growth factors for their ability to modulate cell proliferation in both normal retinas and retinas with lesions. Of the growth factors tested, only the insulin‐related peptides (insulin and insulin‐like growth factors I and II) consistently stimulated proliferation, and this was restricted to the retinal progenitors within the circumferential germinal zone. None of the growth factors tested stimulated proliferation of rod precursors (cells in the mature retina whose progeny are exclusively rod photoreceptors) or the injury‐stimulated retinal progenitors. Although the negative data are subject to multiple interpretations, these data suggest that in the retina of the adult goldfish, insulin‐related peptides regulate proliferation of retinal progenitors within the circumferential germinal zone, but molecules that modulate the proliferation of the rod precursors or injury‐induced retinal progenitors in the retina of the adult goldfish have yet to be identified. J. Comp. Neurol. 394:386–394, 1998. © 1998 Wiley‐Liss, Inc.