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Expression of LOX-1, an Oxidized Low-Density Lipoprotein Receptor, in Experimental Hypertensive Glomerulosclerosis

MIKI NAGASE^*, SHINYA KANAME^*, TAKASHI NAGASE, GANG WANG^*, KATSUYUKI ANDO^*, TATSUYA SAWAMURA^§ and TOSHIRO FUJITA^*

^* Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Tokyo, Japan.
Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
^§ Department of Bioscience, National Cardiovascular Center Research Institute, Suita, Osaka, Japan.

Correspondence to Dr. Miki Nagase, Fourth Department of Internal Medicine, University of Tokyo School of Medicine, 3-28-6 Mejirodai, Bunkyo-ku, Tokyo 112-8688, Japan. Phone: +81-3-3943-1151; Fax: +81-3-3943-3102; E-mail: mnagase-tky{at}umin.ac.jp

Abstract. Oxidized low-density lipoprotein (OxLDL) has been implicated in atherosclerosis and glomerulosclerosis. LOX-1 is a recently identified OxLDL receptor that is abundantly expressed in vascular endothelial cells. The aim of the present study was to investigate LOX-1 expression in the kidneys of hypertensive rats. Dahl salt-sensitive (DS) and salt-resistant (DR) rats were fed a 0.3% or 8% NaCl diet. Some DS 8% rats were treated with manidipine or hydralazine. LOX-1 gene expression was markedly elevated in the kidneys and glomeruli of hypertensive DS 8% rats compared with those of normotensive DR and DS 0.3% rats. Prolonged salt loading further increased the renal LOX-1 expression in DS rats. The LOX-1 upregulation in DS 8% rats was accompanied by renal overexpression of transforming growth factor-ß1 and type I collagen, impaired renal function, and histologic glomerulosclerotic changes, all of which were ameliorated by antihypertensive treatment. LOX-1 was indeed expressed in the glomeruli in vivo and in cultured glomerular cells in vitro. However, LOX-1 expression was elevated in the aorta but not the kidneys of spontaneously hypertensive rats, which exhibited hypertension but minor glomerulosclerotic changes. In conclusion, the LOX-1 upregulation in the kidney of DS 8% rats was parallel to glomerulosclerotic changes and renal dysfunction, suggesting a possible pathogenetic role for renal LOX-1 in the progression to hypertensive glomerulosclerosis.

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