Suppression of renal fibrosis by galectin-1 in high glucose-treated renal epithelial cells

• Published in: Experimental cell research Vol. 316; no. 19; pp. 3282 - 3291
• Main Authors: Okano, Kazuhiro, Tsuruta, Yuki, Yamashita, Tetsuri, Takano, Mari, Echida, Yoshihisa, Nitta, Kosaku
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 15.11.2010; Elsevier BV
• Subjects: 60 APPLIED LIFE SCIENCES; Cell Line; Cellular biology; COLLAGEN; Collagen - genetics; Collagen - metabolism; Collagen Type I; Diabetes; DISEASES; Epithelial Cells - drug effects; Epithelial Cells - enzymology; Epithelial Cells - metabolism; Epithelial Cells - pathology; Extracellular Signal-Regulated MAP Kinases - metabolism; FIBROSIS; Galectin 1 - metabolism; Galectin-1; GLUCOSE; Glucose - pharmacology; GROWTH FACTORS; Humans; INHIBITION; Kidney - drug effects; Kidney - enzymology; Kidney - metabolism; Kidney - pathology; Kidney diseases; KIDNEYS; Kinases; Matrix Metalloproteinase 1 - genetics; Matrix Metalloproteinase 1 - metabolism; Mitogen-activated protein kinase; Models, Biological; Protein Transport - drug effects; Renal fibrosis; Signal transduction; Smad3; Smad3 Protein - metabolism; STIMULATION; TGF-β1; TRANSCRIPTION; Transcription, Genetic - drug effects; TRANSLOCATION; Mitogen-activated protein kinase; Galectin-1; TGF-β1; Smad3; Diabetes; Renal fibrosis

Diabetic nephropathy is the most common cause of chronic kidney disease. We investigated the ability of intracellular galectin-1 (Gal-1), a prototype of endogenous lectin, to prevent renal fibrosis by regulating cell signaling under a high glucose (HG) condition. We demonstrated that overexpression...