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Cellular expression of midkine‐a and midkine‐b during retinal development and photoreceptor regeneration in zebrafish
Author(s) -
Calinescu AndaAlexandra,
Vihtelic Thomas S.,
Hyde David R.,
Hitchcock Peter F.
Publication year - 2009
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/cne.22031
Subject(s) - midkine , biology , zebrafish , muller glia , retina , microbiology and biotechnology , retinal regeneration , regeneration (biology) , retinal , embryonic stem cell , stem cell , progenitor cell , neuroscience , growth factor , genetics , receptor , gene , biochemistry
In the retina of adult teleosts, stem cells are sustained in two specialized niches: the ciliary marginal zone (CMZ) and the microenvironment surrounding adult Müller glia. Recently, Müller glia were identified as the regenerative stem cells in the teleost retina. Secreted signaling molecules that regulate neuronal regeneration in the retina are largely unknown. In a microarray screen to discover such factors, we identified midkine‐b ( mdkb ). Midkine is a highly conserved heparin‐binding growth factor with numerous biological functions. The zebrafish genome encodes two distinct midkine genes: mdka and mdkb. Here we describe the cellular expression of mdka and mdkb during retinal development and the initial, proliferative phase of photoreceptor regeneration. The results show that in the embryonic and larval retina mdka and mdkb are expressed in stem cells, retinal progenitors, and neurons in distinct patterns that suggest different functions for the two molecules. Following the selective death of photoreceptors in the adult, mdka and mdkb are coexpressed in horizontal cells and proliferating Müller glia and their neurogenic progeny. These data reveal that Mdka and Mdkb are signaling factors present in the retinal stem cell niches in both embryonic and mature retinas, and that their cellular expression is actively modulated during retinal development and regeneration. J. Comp. Neurol. 514:1–10, 2009. © 2009 Wiley‐Liss, Inc.