HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Submit a response View responses Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Nishiguchi, K. M. Articles by Terasaki, H. Search for Related Content PubMed PubMed Citation Articles by Nishiguchi, K. M. Articles by Terasaki, H.

The Role of VEGF and VEGFR2/Flk1 in Proliferation of Retinal Progenitor Cells in Murine Retinal Degeneration

From the Department of Ophthalmology, Nagoya University Graduate School of Medicine, Nagoya, Japan.

PURPOSE. To analyze the role of VEGF and its receptors, VEGFR2/Flk1 and VEGFR1/Flt1, on retinal progenitor cells (RPCs) in a murine model of inherited retinal degeneration (rd1 mice).

METHODS. After proliferating RPCs in the retina of rd1 mice were labeled with bromodeoxyuridine (BrdU), expressions of VEGFR2/Flk1 and VEGFR1/Flt1 were immunohistochemically analyzed. To examine its effect on the proliferation of BrdU-positive RPCs in rd1 mice, VEGF was administered into retinal culture medium with or without blocking agents against VEGFR2/Flk1 or VEGFR1/Flt1 in vitro or injected into vitreous cavity in vivo.

RESULTS. BrdU-labeled RPCs in rd1 mice expressed VEGFR2/Flk1 but not VEGFR1/Flt1. These cells later expressed retinal neuronal markers such as Pax6 and rhodopsin. Exposure of the retinas from postnatal day (P) 9 rd1 mice to VEGF increased the number of proliferating RPCs by 61% in vitro. This effect was blocked by concomitant administration of VEGFR2/Flk1 kinase inhibitor. In vivo, a single intravitreal injection of VEGF in rd1 mice at P9 increased by 138% the number of RPCs and cells that developed from RPCs in the peripheral retina at P18.

CONCLUSIONS. VEGF stimulates the proliferation of RPCs through VEGFR2/Flk1 in rd1 mice. The observed proliferation of RPCs that have the potential to differentiate into retinal neurons may enhance the regeneration of the degenerating retina.

This article has been cited by other articles:

				M. Saint-Geniez, T. Kurihara, and P. A. D'Amore Role of Cell and Matrix-Bound VEGF Isoforms in Lens Development Invest. Ophthalmol. Vis. Sci., January 1, 2009; 50(1): 311 - 321. [Abstract] [Full Text] [PDF]

				H. Kaneko, K. M. Nishiguchi, M. Nakamura, S. Kachi, and H. Terasaki Characteristics of Bone Marrow-Derived Microglia in the Normal and Injured Retina Invest. Ophthalmol. Vis. Sci., September 1, 2008; 49(9): 4162 - 4168. [Abstract] [Full Text] [PDF]

				H. Kaneko, K. M. Nishiguchi, M. Nakamura, S. Kachi, and H. Terasaki Retardation of Photoreceptor Degeneration in the Detached Retina of rd1 Mouse Invest. Ophthalmol. Vis. Sci., February 1, 2008; 49(2): 781 - 787. [Abstract] [Full Text] [PDF]

				K. M. Nishiguchi, H. Kaneko, M. Nakamura, S. Kachi, and H. Terasaki Identification of Photoreceptor Precursors in the Pars Plana during Ocular Development and after Retinal Injury Invest. Ophthalmol. Vis. Sci., January 1, 2008; 49(1): 422 - 428. [Abstract] [Full Text] [PDF]

eLetters: