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SSEA-1 marks regionally restricted immature subpopulations of embryonic retinal progenitor cells that are regulated by the Wnt signaling pathway

Authors :
Koso, Hideto
Ouchi, Yasuo
Tabata, Yoko
Aoki, Yutaka
Satoh, Shinya
Arai, Ken-Ichi
Watanabe, Sumiko
Source :
Developmental Biology. April 1, 2006, Vol. 292 Issue 1, p265, 12 p.
Publication Year :
2006

Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2005.09.051 Byline: Hideto Koso, Yasuo Ouchi, Yoko Tabata, Yutaka Aoki, Shinya Satoh, Ken-ichi Arai, Sumiko Watanabe Keywords: Retina; Mouse; Progenitor cells; FACS; SSEA-1; Proliferation; Differentiation Abstract: Identification and expansion of retinal progenitor cells are critical issues from both scientific and clinical aspects. Here, we identified SSEA-1 (CD15) as a novel surface antigen that can be used to define immature retinal progenitor cells. SSEA-1-expressing retinal cells were found in the peripheral region of the early embryonic mouse retina, and then their number dramatically disappeared along with retinal development. FACS analysis showed that the cells strongly positive for SSEA-1 co-expressed Ki67 proliferation antigen in all the developmental stages examined. The SSEA-1-expressing cells formed larger colonies than the non-expressing ones in retinal re-aggregation cultures. Moreover, late onset of rhodopsin expression was observed in SSEA-1-positive progenitor cells, supporting the idea that these cells have an intrinsically immature character. Differential expression of Wnt signal-related genes between SSEA-1-positive and -negative subpopulations of retina cells was revealed, and the expression of constitutively active forms of Wnt signaling molecules resulted in a greater number of SSEA-1-positive cells. In light of all of the data taken together, we propose SSEA-1 to be a surface marker to define a regionally restricted immature subset of progenitor cells of mouse neural retina, with SSEA-1 expression by them positively regulated by Wnt signals. Author Affiliation: Department of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan Article History: Received 2 August 2005; Revised 16 September 2005; Accepted 30 September 2005

Details

Language :
English
ISSN :
00121606
Volume :
292
Issue :
1
Database :
Gale General OneFile
Journal :
Developmental Biology
Publication Type :
Academic Journal
Accession number :
edsgcl.194112898