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Legumain/asparaginyl endopeptidase (EC 3.4.22.34) is a novel cysteine protease that is abundantly expressed in the late endosomes and lysosomes of renal proximal tubular cells. Recently, emerging evidence has indicated that legumain might play an important role in control of extracellular matrix turnover in various pathological conditions such as tumor growth/metastasis and progression of atherosclerosis. We initially found that purified legumain can directly degrade fibronectin, one of the main components of the extracellular matrix, in vitro. Therefore, we examined the effect of legumain on fibronectin degradation in cultured mouse renal proximal tubular cells. Fibronectin processing can be inhibited by chloroquine, an inhibitor of lysosomal degradation, and can be enhanced by the overexpression of legumain, indicating that fibronectin degradation occurs in the presence of legumain in lysosomes from renal proximal tubular cells. Furthermore, in legumain-deficient mice, unilateral ureteral obstruction (UUO)-induced renal interstitial protein accumulation of fibronectin and renal interstitial fibrosis were markedly enhanced. These findings indicate that legumain might have an important role in extracellular matrix remodeling via the degradation of fibronectin in renal proximal tubular cells.

Corrigendum to ‘‘Legumain/asparaginyl endopeptidase controls extracellular matrix remodeling through the degradation of fibronectin in mouse renal proximal tubular cells’’ [FEBS Lett. 581 (2007) 1417–1424] Yoshikata Morita, Hisazumi Araki, Toshiro Sugimoto*, Keisuke Takeuchi, Takuya Yamane, Toshinaga Maeda, Yoshio Yamamoto, Katsuji Nishi, Masahide Asano, Kanae Shirahama-Noda, Mikio Nishimura, Takashi Uzu, Ikuko Hara-Nishimura, Daisuke Koya, Atsunori Kashiwagi, Iwao Ohkubo a Department of Medical Biochemistry, Shiga University of Medical Science, Seta, Otsu 520-2192, Japan b Department of Internal Medicine, Shiga University of Medical Science, Seta, Otsu 520-2192, Japan c Legal Medicine, Shiga University of Medical Science, Seta, Otsu 520-2192, Japan d Division of Endocrinology and Metabolism, Kanazawa Medical University, Ishikawa 920-0293, Japan e Advanced Science Research Center, Kanazawa University, Takaramachi, Kanazawa 920-8640, Japan f Department of Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan g Graduate School of Science, Kyoto University, Kitashirakawa, Sakyo-ku, Kyoto 606-8502, Japan