title: Alteration in the phenotype of macrophages in the repair of renal interstitial fibrosis in mice.
abstract: OBJECTIVE
  Renal interstitial fibrosis is the final common pathway determining long-term prognosis of chronic kidney diseases, but its repair process is scarcely understood. Because recent reports indicate that M2 macrophages play important roles in the repair of various tissues, special attention was paid to the phenotypes of infiltrating macrophages in the present study when the histological changes occurring in mouse kidneys after the release of unilateral ureteral obstruction (UUO) inducing renal fibrosis were analyzed.
  
  
  METHODS
  The left ureter of male mice was obstructed for 10 days by using a vascular clamp, and that kidney was removed for analysis either on the day when the clamp was removed or after the kidney had been allowed to recover for 3, 7 or 21 days.
  
  
  RESULTS
  Interstitial fibrosis assessed by picrosirius red staining decreased with time after the release, and this decrease was paralleled by a decrease in the interstitial area positive for α-smooth muscle actin. Macrophage infiltration assessed by F4/80 staining also significantly decreased from day 3. In contrast, real-time reverse transcription polymerase chain reaction revealed that the ratios of mRNA for the macrophage scavenger receptor (CD204) and the mannose receptor (CD206), both of which are preferentially expressed on M2 macrophages, to CD68 (a general macrophage marker) were significantly greater on day 7 than on day 0 in the UUO-released mice.
  
  
  CONCLUSIONS
  Although the total number of infiltrating myofibroblasts and macrophages decreased after UUO release, the ratios of macrophages expressing CD204 and CD206 increased, suggesting that M2 macrophages play an important role in the repair of renal fibrosis.
authors.affiliation: Department of Nephrology, National Defence Medical College, Tokorozawa, Saitama, Japan. dr21023@ndmc.ac.jp
authors.forename: Taketoshi
authors.initials: T
authors.lastname: Kushiyama
authors.forename: Takashi
authors.initials: T
authors.lastname: Oda
authors.forename: Muneharu
authors.initials: M
authors.lastname: Yamada
authors.forename: Keishi
authors.initials: K
authors.lastname: Higashi
authors.forename: Kojiro
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Sakurai
authors.forename: Soichiro
authors.initials: S
authors.lastname: Miura
authors.forename: Hiroo
authors.initials: H
authors.lastname: Kumagai
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000235:genetics; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics; D049109:Cell Proliferation; D005355:Fibrosis; D016753:Interleukin-10 / Q000032:analysis; D007668:Kidney / Q000473:pathology*; D037181:Lectins, C-Type / Q000032:analysis; D008264:Macrophages / Q000502:physiology*; D008297:Male; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000032:analysis; D051379:Mice; D008810:Mice, Inbred C57BL; D058628:Myofibroblasts / Q000502:physiology; D010641:Phenotype; D012333:RNA, Messenger / Q000032:analysis; D011956:Receptors, Cell Surface / Q000032:analysis; D051117:Scavenger Receptors, Class A / Q000032:analysis; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D016753:Interleukin-10; D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D051117:Scavenger Receptors, Class A; C081026:CD68 protein, mouse; D000097382:CD68 Molecule; C495140:Msr1 protein, mouse