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TISSUE-SPECIFIC STEM CELLS

CD138/Syndecan-1 and SSEA-1 Mark Distinct Populations of Developing Ciliary Epithelium That Are Regulated Differentially by Wnt Signal

^aDepartment of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, Tokyo, Japan;
^bDepartment of Pharmacology, Graduate School of Medicine, Kyoto University, Kyoto, Japan

Key Words. CD antigen • Retina • Ciliary epithelium • β-Catenin signal • Mouse

Correspondence: Correspondence: Sumiko Watanabe, Ph.D., Department of Molecular and Developmental Biology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. Telephone: 81-3-5449-5663; Fax: 81-3-5449-5474; e-mail: sumiko{at}ims.u-tokyo.ac.jp

Received on March 28, 2008; accepted for publication on August 22, 2008.

First published online in STEM CELLS EXPRESS  September 11, 2008.

Ciliary epithelium (CE), which consists of nonpigmented and pigmented layers, develops from the optic vesicle. However, the molecular mechanisms underlying CE development have not been closely examined, in part because cell-surface markers suitable for specific labeling of subregions of the retina were unknown. Here, we identified CD138/syndecan-1 and stage specific embryonic antigen-1 (SSEA-1) CD15 as cell-surface antigens marking nonpigmented and pigmented CE, respectively. During retinal development, both CD138 and SSEA-1 were expressed in the early stage, and segregation of these markers in the tissue began at around embryonic day (E) 10. As a result, CD138-positive (CD138+) cells were found at the most distal tip of the retina, and SSEA-1+ cells were found in the periphery adjacent to the area of CD138 expression. In vitro characterization of isolated CD138+ or SSEA-1+ cell subpopulations revealed that CD138+ cells lose their retinal progenitor characteristics between E13 and E16, suggesting that they commit to becoming nonpigmented CE cells within this period. By in vivo mouse models, we found that stabilized β-catenin expanded the area of CD138+ nonpigmented CE and that elimination of β-catenin inhibited development of nonpigmented CE cells. These findings are the first to use cell-surface markers to ascertain the spatial and temporal transitions that occur in developing CE.

Disclosure of potential conflicts of interest is found at the end of this article.