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Insulin‐related growth factors stimulate proliferation of retinal progenitors in the goldfish
Author(s) -
Boucher ShayneEmile M.,
Hitchcock Peter F.
Publication year - 1998
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19980511)394:3<386::aid-cne9>3.0.co;2-y
Subject(s) - biology , retina , progenitor cell , neurogenesis , retinal , microbiology and biotechnology , muller glia , retinal regeneration , insulin , regeneration (biology) , progenitor , neuroscience , endocrinology , stem cell , biochemistry
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.