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IFN-Inducible Protein-10 Has a Differential Role in Podocyte during Thy 1.1 Glomerulonephritis

Gi Dong Han^*, Hiroko Koike^*, Takeshi Nakatsue^*, Kenji Suzuki, Hiroyuki Yoneyama, Shosaku Narumi, Naoto Kobayashi, Peter Mundel^||, Fujio Shimizu^* and Hiroshi Kawachi^*

*Department of Cell Biology, Institute of Nephrology, Division of Gastroenterology and Hepatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan; Department of Molecular Preventive Medicine, School of Medicine and Core Research and Evolutional Science and Technology, University of Tokyo, Tokyo, Japan; Department of Anatomy and Embryology, Ehime University School of Medicine, Ehime, Japan; and ^||Division of Nephrology, Albert Einstein College of Medicine, Bronx, New York

Correspondence to Dr. Hiroshi Kawachi, Department of Cell Biology, Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi-dori, Niigata, 951-8510, Japan. Phone: +81-25-227-2160; Fax: +81-25-227-0770; E-mail: kawachi{at}med.niigata-u.ac.jp

ABSTRACT. IFN-inducible protein-10 (IP-10/CXCL10) is a potent chemoattractant for activated T lymphocytes and was recently reported to have several additional biologic activities. In this study, the expression and the function in normal glomeruli and in Thy1.1 glomerulonephritis (GN) were investigated. The expression of IP-10 was detected in normal rat glomeruli mainly in the podocyte. The expression of IP-10 was also detected on the cultured podocyte. The IP-10 expression was elevated at the early phase of Thy1.1 GN. The double staining immunofluorescence study clearly demonstrated that the elevated expression of IP-10 was mostly detected in the podocyte and very partly in mesangial area. A receptor for IP-10, CXCR3, showed similar expression patterns to that of IP-10. Expressions of neither of IP-10 nor of CXCR3 were detected on the inflammatory cells. For elucidating the role of IP-10, the blocking study was carried out with monoclonal anti–IP-10 antibody. The monoclonal anti–IP-10 antibody treatment decreased the expression of IP-10 and podocyte-associated proteins such as nephrin and podocin that are reported to be essential for maintaining the podocyte function (IP-10, 53.0% to control; nephrin, 43.5%; podocin, 60.4%). The findings indicated that the anti–IP-10 treatment disturbed the podocyte function. The anti–IP-10 treatment given to the rats with Thy1.1 nephritis exacerbated proteinuria, mesangiolysis, and matrix expansion. Collectively, the findings indicated that IP-10 plays a role in maintaining the podocyte function. Also, the findings suggested that anti–IP-10 treatment exacerbated the glomerular alterations in Thy1.1 GN by disturbing the podocyte function.

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