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NDT Advance Access originally published online on May 27, 2009
Nephrology Dialysis Transplantation 2009 24(10):3006-3012; doi:10.1093/ndt/gfp243
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© The Author [2009]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Induction of nephrin gene expression by selective cooperation of the retinoic acid receptor and the vitamin D receptor

Maro Okamura, Yosuke Takano, Yukinori Saito, Jian Yao and Masanori Kitamura

Department of Molecular Signaling, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi 409-3898, Japan

Correspondence and offprint requests to: Masanori Kitamura; E-mail: masanori{at}yamanashi.ac.jp



  Abstract

Background. Nephrin is a key molecule involved in the structure and function of the slit diaphragm in the glomerulus. We previously reported that all-trans retinoic acid (ATRA) and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] induced expression of nephrin in murine podocytes. In this report, we investigated roles of the retinoic acid receptor (RAR), the retinoid X receptor (RXR) and the vitamin D receptor (VDR) in the regulation of the nephrin gene.

Methods. Reporter podocytes were treated with agonists and/or antagonists of RAR, RXR or VDR, and activities of the nephrin gene promoter, the retinoic acid response element (RARE) and the vitamin D response element (VDRE) were evaluated.

Results. Expression of nephrin in podocytes was up-regulated by ATRA and 1,25(OH)2D3. The nephrin gene promoter was also activated by these agents, which was mediated by RAR and VDR, but unexpectedly, not by RXR. ATRA-triggered, RAR-mediated activation of the nephrin gene promoter was not suppressed by the VDR antagonist. Similarly, ATRA-induced activation of RARE was not inhibited by the VDR antagonist. In contrast, the 1,25(OH)2D3-triggered, VDR-mediated activation of the nephrin gene promoter was significantly suppressed by the RAR antagonist, but not by RXR antagonists. Interestingly, 1,25(OH)2D3-induced activation of VDRE was not inhibited by the RAR antagonist.

Conclusions. These results suggested selective cooperation of RAR and VDR in the regulation of the nephrin gene, i.e. (1) ATRA induces nephrin gene expression via RAR independently of RXR and VDR and (2) 1,25(OH)2D3 induces nephrin gene expression via selective cooperation of RAR and VDR, which is independent of RXR.

Keywords: nephrin; podocyte; retinoic acid receptor (RAR); retinoic acid; vitamin D receptor (VDR)

Received for publication: 6. 3.09
Accepted in revised form: 30. 4.09


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