title: SAMP1/Sku as a murine model for tubulointerstitial nephritis: a study using unilateral ureteral obstruction.
abstract: The SAMP1/Sku mouse is a substrain of the SAMP1 (senescence-accelerated-mouse prone 1) which exhibits renal mononuclear cell infiltration from a younger age. We hypothesized that this renal characteristic is related to the incidence of tubulointerstitial nephritis (TIN). The purpose of the present study was to evaluate the applicability of the SAMP1/Sku mouse as a murine model for TIN. TIN was experimentally induced by unilateral ureteral obstruction (UUO). The SAMP1/Sku and control ICR of both sexes received either a sham or UUO operation and were sacrificed 7 days after the operation. The kidneys of the mice were observed histopathologically, immunohistochemically and semiquantitatively. UUO kidneys showed mononuclear cell infiltration, tubular atrophy and interstitial fibrosis. In males, semiquantitative scores of mononuclear cell infiltration, tubular atrophy, and F4/80, alpha-smooth muscle actin (alpha-SMA) and transforming growth factor (TGF)-beta1 reactions were significantly higher in SAMP1/Sku than in ICR. Likewise, in females, tubular atrophy and F4/80 reaction scores were significantly higher in SAMP1/Sku than in ICR. In conclusion, induction of TIN damage by UUO was more serious in SAMP1/Sku mice than in ICR. Therefore, we propose that SAMP1/Sku mice, especially male SAMP1/Sku, have congenital risk factors for the development of TIN.
authors.affiliation: Laboratory of Veterinary Anatomy, Faculty of Agriculture, Kagoshima University, Korimoto, Japan.
authors.forename: Akira
authors.initials: A
authors.lastname: Yabuki
authors.forename: Michie
authors.initials: M
authors.lastname: Maeda
authors.forename: Mitsuharu
authors.initials: M
authors.lastname: Matsumoto
authors.forename: Ryozo
authors.initials: R
authors.lastname: Kamimura
authors.forename: Taku
authors.initials: T
authors.lastname: Masuyama
authors.forename: Syusaku
authors.initials: S
authors.lastname: Suzuki
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D001284:Atrophy; D004195:Disease Models, Animal; D005260:Female; D005355:Fibrosis; D007150:Immunohistochemistry; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D009336:Necrosis; D009395:Nephritis, Interstitial / Q000209:etiology; D012307:Risk Factors; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014517:Ureteral Obstruction / Q000150:complications / Q000378:metabolism / Q000473:pathology
chemical_list: D000199:Actins; D000943:Antigens, Differentiation; D016212:Transforming Growth Factor beta; C036763:monocyte-macrophage differentiation antigen