2007 JASN IMPACT FACTOR 7.111	HOME   AUTHOR INFO   EDITORIAL BOARD   SUBSCRIBE   FEEDBACK   ALERTS   HELP
advanced	CURRENT ISSUE	ARCHIVES	JASN Express	ONLINE SUBMISSION

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal 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 Google Scholar Google Scholar Articles by Sawai, K. Articles by Nakao, K. Search for Related Content PubMed PubMed Citation Articles by Sawai, K. Articles by Nakao, K.

Angiogenic Protein Cyr61 is Expressed by Podocytes in Anti-Thy-1 Glomerulonephritis

Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, Kyoto, Japan.

Correspondence to Dr. Kiyoshi Mori, Department of Medicine and Clinical Science, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. Phone: 81-75-751-4286; Fax: 81-75-771-9452;

ABSTRACT. Dynamic recovery of glomerular structure occurs after severe glomerular damage in anti-Thy-1 glomerulonephritis (Thy-1 GN), but its mechanism remains to be investigated. To identify candidate genes possibly involved in glomerular reconstruction, screening was performed for genes that are specifically expressed by podocytes and are upregulated in glomeruli of Thy-1 GN. Among them, cysteine-rich protein 61 (Cyr61 or CCN1), a soluble angiogenic protein belonging to the CCN family, was identified. By Northern blot analysis, Cyr61 mRNA was markedly upregulated in glomeruli of Thy-1 GN from day 3 through day 7, when mesangial cell migration was most prominent. By in situ hybridization and immunohistochemistry, Cyr61 mRNA and protein were expressed by proximal straight tubules and afferent and efferent arterioles in normal rat kidneys and were intensely upregulated at podocytes in Thy-1 GN. Platelet-derived growth factor–BB (PDGF-BB) and transforming growth factor–1 (TGF-1), of which the gene expression in the glomeruli of Thy-1 GN was upregulated in similar time course as Cyr61, induced Cyr61 mRNA expression in cultured podocytes. Furthermore, supernatant of Cyr61-overexpressing cells inhibited PDGF-induced mesangial cell migration. In conclusion, it is shown that Cyr61 is strongly upregulated at podocytes in Thy-1 GN possibly by PDGF and TGF-. Cyr61 may be involved in glomerular remodeling as a factor secreted from podocytes to inhibit mesangial cell migration. E-mail: keyem@kuhp.kyoto-u.ac.jp

This article has been cited by other articles:

				K. Sawai, M. Mukoyama, K. Mori, M. Kasahara, M. Koshikawa, H. Yokoi, T. Yoshioka, Y. Ogawa, A. Sugawara, H. Nishiyama, et al. Expression of CCN1 (CYR61) in developing, normal, and diseased human kidney Am J Physiol Renal Physiol, October 1, 2007; 293(4): F1363 - F1372. [Abstract] [Full Text] [PDF]

				M. Koshikawa, M. Mukoyama, K. Mori, T. Suganami, K. Sawai, T. Yoshioka, T. Nagae, H. Yokoi, H. Kawachi, F. Shimizu, et al. Role of p38 Mitogen-Activated Protein Kinase Activation in Podocyte Injury and Proteinuria in Experimental Nephrotic Syndrome J. Am. Soc. Nephrol., September 1, 2005; 16(9): 2690 - 2701. [Abstract] [Full Text] [PDF]

				H. Yokoi, M. Mukoyama, T. Nagae, K. Mori, T. Suganami, K. Sawai, T. Yoshioka, M. Koshikawa, T. Nishida, M. Takigawa, et al. Reduction in Connective Tissue Growth Factor by Antisense Treatment Ameliorates Renal Tubulointerstitial Fibrosis J. Am. Soc. Nephrol., June 1, 2004; 15(6): 1430 - 1440. [Abstract] [Full Text] [PDF]

				R. Abramovitch, E. Tavor, J. Jacob-Hirsch, E. Zeira, N. Amariglio, O. Pappo, G. Rechavi, E. Galun, and A. Honigman A Pivotal Role of Cyclic AMP-Responsive Element Binding Protein in Tumor Progression Cancer Res., February 15, 2004; 64(4): 1338 - 1346. [Abstract] [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673