title: Renal fibroblast-like cells in Goodpasture syndrome rats.
abstract: BACKGROUND
  The extent of renal fibrosis is the best predictor for functional outcomes in a variety of progressive renal diseases. Interstitial fibroblast-like cells (FbLCs) are presumably involved in the fibrotic process. However, such FbLCs have never been well characterized in the kidney.
  
  
  METHODS
  We characterized renal FbLCs in the nephritic kidney (in which the number of FbLCs and extracellular matrix accumulation were significantly increased) with regards to their expression of phenotypic and functional markers using day 49 Goodpasture syndrome (GPS) rats.
  
  
  RESULTS
  Within the renal cortical interstitium, there were a number of alpha-smooth muscle actin(+) (alpha-SMA(+)) FbLCs, negative for vimentin (VIM) and transforming growth factor-beta 1, and not equipped with well-developed rough endoplasmic reticulum and actin-stress fibers. All of these findings were incompatible with the typical features of granulation tissue alpha-SMA(+) myofibroblasts. On the other hand, FbLCs negative for alpha-SMA and VIM produced alpha1(I) procollagen in the nephritic kidney.
  
  
  CONCLUSIONS
  A number of FbLC populations reside within the cortical interstitium of the kidney in GPS rats, each of which is likely to have developed independently in response to the local conditions of the nephritic kidney, contributing to renal fibrogenesis. Further studies are needed to clarify the key type of FbLC that orchestrates other members to produce renal fibrosis.
authors.affiliation: Department of Nephrology, Saitama Medical College, Irumagun, Saitama, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Okada
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: Y
authors.initials: Y
authors.lastname: Kanno
authors.forename: T
authors.initials: T
authors.lastname: Kobayashi
authors.forename: S
authors.initials: S
authors.lastname: Ban
authors.forename: R
authors.initials: R
authors.lastname: Kalluri
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
mesh_terms: D000199:Actins / Q000032:analysis; D000818:Animals; D019867:Anti-Glomerular Basement Membrane Disease / Q000473:pathology* / Q000503:physiopathology*; D019898:Autocrine Communication; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000473:pathology / Q000502:physiology; D005347:Fibroblasts / Q000737:chemistry / Q000473:pathology / Q000648:ultrastructure; D005355:Fibrosis; D015870:Gene Expression; D007668:Kidney / Q000473:pathology*; D016253:Microscopy, Immunoelectron; D019899:Paracrine Communication; D010641:Phenotype; D011347:Procollagen / Q000235:genetics; D020574:Proto-Oncogene Proteins c-sis / Q000032:analysis; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D016212:Transforming Growth Factor beta / Q000032:analysis; D053773:Transforming Growth Factor beta1; D014746:Vimentin / Q000032:analysis
chemical_list: D000199:Actins; D011347:Procollagen; D020574:Proto-Oncogene Proteins c-sis; D012333:RNA, Messenger; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; D014746:Vimentin