title: Up-regulation of galectin-3 in acute renal failure of the rat.
abstract: Galectin-3, a multifunctional beta-galactoside-binding lectin, is known to participate in development, oncogenesis, cell-to-cell attachment, and inflammation. We studied to determine whether galectin-3 is associated with cell injury and regeneration in two types of acute renal failure (ARF), namely ischemic and toxic ARF. In ischemia/reperfusion renal injury in rats (bilateral renal pedicles clamped for 40 minutes), galectin-3 mRNA began to increase at 2 hours and extended by 6.2-fold at 48 hours (P: < 0.01 versus normal control rats), and then decreased by 28 days after injury. In addition, a significant negative correlation between galectin-3 mRNA expression and serum reciprocal creatinine was shown at 48 hours after injury (n = 13, r = -0.94, P: < 0.0001). In folic acid-induced ARF, galectin-3 mRNA was found to be up-regulated at 2 hours after injury and increased levels continued until at least 7 days post-injury. In immunohistochemistry, at 2 hours following reperfusion, galectin-3 began to develop in proximal convoluted tubules. From 6 hours up to 48 hours, galectin-3 was also found in proximal straight tubules, distal tubules, thick ascending limbs, and collecting ducts. In later stages of regeneration, galectin-3 expressions were found in macrophages. In conclusion, we demonstrated that galectin-3 expressions were markedly up-regulated in both ischemic and toxic types of ARF. Galectin-3 may play an important role in acute tubular injury and the following regeneration stage.
authors.affiliation: Second Department of Medicine, National Defense Medical College, Tokorozawa, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Nishiyama
authors.forename: S
authors.initials: S
authors.lastname: Kobayashi
authors.forename: A
authors.initials: A
authors.lastname: Ishida
authors.forename: I
authors.initials: I
authors.lastname: Nakabayashi
authors.forename: O
authors.initials: O
authors.lastname: Tajima
authors.forename: S
authors.initials: S
authors.lastname: Miura
authors.forename: M
authors.initials: M
authors.lastname: Katayama
authors.forename: H
authors.initials: H
authors.lastname: Nogami
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D000943:Antigens, Differentiation / Q000235:genetics / Q000378:metabolism*; D003404:Creatinine / Q000097:blood; D005492:Folic Acid / Q000633:toxicity; D037502:Galectin 3; D007124:Immunoenzyme Techniques; D007668:Kidney / Q000187:drug effects / Q000473:pathology / Q000601:surgery; D037102:Lectins / Q000235:genetics / Q000378:metabolism*; D008297:Male; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D015854:Up-Regulation
chemical_list: D000943:Antigens, Differentiation; D037502:Galectin 3; D037102:Lectins; D012333:RNA, Messenger; D005492:Folic Acid; D003404:Creatinine