title: Matrix remodelling in dilated cardiomyopathy entails the occurrence of oncofetal fibronectin molecular variants.
abstract: OBJECTIVE
  To investigate whether disturbance of the cellular homoeostasis and integrity of cardiomyocytes in dilated cardiomyopathy (DCM) is accompanied by alterations in cell-matrix relations as indicated by changes in the deposition of fibronectin (FN) isoforms.
  
  
  METHODS
  Tissue from a case series of patients with DCM was investigated by immunohistochemistry with antibodies against FN (all variants, clone IST4), ED-A+ FN (clone IST9), ED-B+ FN (clone BC1), and oncofetal glycosylated FN (clone 5C10). The sites of de novo synthesis of FN were demonstrated by means of non-radioactive RNA in situ hybridisation (ISH) with biotinylated FN cDNA fragments as the probe.
  
  
  METHODS
  University hospital.
  
  
  METHODS
  Samples from 10 patients with clinical criteria and histological diagnosis of DCM and from 3 individuals with normal hearts.
  
  
  METHODS
  Samples were obtained by right ventricular endomyocardial biopsy.
  
  
  METHODS
  Distribution of oncofetal FN variants in DCM hearts.
  
  
  RESULTS
  Immunostaining of FN (IST4, all variants) showed a coarse interstitial network in normal and diseased myocardium. ED-A+ FN was deposited as fine interstitial spots in normal myocardium and in DCM samples. Immunostaining for oncofetal glycosylated FN and ED-B+ FN was not seen in normal adult myocardium, whereas myocardium from DCM patients showed focal and delicate staining in the interstitium. RNA ISH showed that these deposits resulted from local FN synthesis.
  
  
  CONCLUSIONS
  The results accord with de novo expression of oncofetal FN variants in hearts from patients with DCM. The oncofetal FN variants may serve as disease markers in myocardium affected by DCM.
authors.affiliation: Institute of Pathology, University of Jena, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Gabler
authors.forename: A
authors.initials: A
authors.lastname: Berndt
authors.forename: H
authors.initials: H
authors.lastname: Kosmehl
authors.forename: U
authors.initials: U
authors.lastname: Mandel
authors.forename: L
authors.initials: L
authors.lastname: Zardi
authors.forename: S
authors.initials: S
authors.lastname: Müller
authors.forename: A
authors.initials: A
authors.lastname: Stelzner
authors.forename: D
authors.initials: D
authors.lastname: Katenkamp
mesh_terms: D000328:Adult; D017398:Alternative Splicing; D000911:Antibodies, Monoclonal; D002311:Cardiomyopathy, Dilated / Q000378:metabolism* / Q000473:pathology; D005109:Extracellular Matrix / Q000378:metabolism*; D005353:Fibronectins / Q000032:analysis* / Q000235:genetics / Q000378:metabolism; D005355:Fibrosis; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007536:Isomerism; D008957:Models, Genetic; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis
chemical_list: D000911:Antibodies, Monoclonal; D005353:Fibronectins; D012333:RNA, Messenger