title: Tissue models of peritoneal fibrosis.
abstract: OBJECTIVE
  To evaluate the utility of peritoneal pathologic samples, unrelated to peritoneal dialysis (PD) treatment, for the study of peritoneal fibrosis and inflammation.
  
  
  METHODS
  Comparative morphologic and immunohistochemical study of peritoneal pathologic samples unrelated to PD with peritoneal biopsies from PD patients with special emphasis on the expression of myofibroblastic and epithelial-to-mesenchymal transition markers.
  
  
  RESULTS
  Regarding morphology, PD-related simple fibrosis was less cellular, with greater stromal hyalinization, determining a homogeneous, hypocellular aspect of the submesothelium. In contrast, non-PD fibrosis was more cellular with an extracellular matrix showing a dense and fibrillar quality with wide bundles of collagen. Hylinazing vasculopathy was only present in PD samples. Myofibroblastic differentiation and epithelial-to-mesenchymal transition were common findings in all situations of peritoneal fibrosis. Calponin and calretinin are useful cellular markers to study such fibrogenic mechanisms and correlate with other well-known markers such as a -SMA and cytokeratins. Their expression was much more intense in those samples showing acute inflammation (peritonitis).
  
  
  CONCLUSIONS
  Non-PD models of peritoneal fibrosis seem very useful to evaluate important features of human peritoneal pathology such us fibrogenesis, and inflammation. Fibrogenic events such as myofibroblastic differentiation and epithelial-to-mesenchymal transition are evident in these tissue samples allowing us to use them as an accessible source for in vivo and ex vivo studies. Both events show their maximal expression in situations of acute inflammation supporting the important role that peritonitis episodes play in the progression of fibrosis.
authors.affiliation: Department of Pathology, University Hospital, 19002 Guadalajara, Spain. jjhefferman@yahoo.com
authors.forename: J A
authors.initials: JA
authors.lastname: Jimenez-Heffernan
authors.forename: A
authors.initials: A
authors.lastname: Cirugeda
authors.forename: M A
authors.initials: MA
authors.lastname: Bajo
authors.forename: G
authors.initials: G
authors.lastname: Del Peso
authors.forename: M L
authors.initials: ML
authors.lastname: Perez-Lozano
authors.forename: C
authors.initials: C
authors.lastname: Perna
authors.forename: R
authors.initials: R
authors.lastname: Selgas
authors.forename: M
authors.initials: M
authors.lastname: Lopez-Cabrera
mesh_terms: D000199:Actins / Q000378:metabolism; D015415:Biomarkers; D001706:Biopsy; D064032:Calbindin 2; D002135:Calcium-Binding Proteins / Q000378:metabolism; D016022:Case-Control Studies; D002454:Cell Differentiation; D004487:Edema / Q000473:pathology; D004848:Epithelium / Q000378:metabolism* / Q000473:pathology*; D005337:Fibrin / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology; D005355:Fibrosis; D006552:Hernia, Inguinal / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006818:Hyalin / Q000378:metabolism; D007633:Keratins / Q000378:metabolism; D008840:Microfilament Proteins; D009504:Neutrophils / Q000378:metabolism; D010537:Peritoneum / Q000473:pathology*; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D012598:Sclerosis; D000267:Tissue Adhesions / Q000378:metabolism / Q000473:pathology; D000096985:Calponins
chemical_list: D000199:Actins; D015415:Biomarkers; D064032:Calbindin 2; D002135:Calcium-Binding Proteins; D005337:Fibrin; D007633:Keratins; D008840:Microfilament Proteins; D064030:S100 Calcium Binding Protein G; D000096985:Calponins; C576764:CALB2 protein, human