title: Mediators of perivascular inflammation in the left ventricle of renovascular hypertensive rats.
abstract: OBJECTIVE
  Inflammatory cells invade the fibrotic myocardium of spontaneously hypertensive rats at the same sites as where fibroblasts are produced. The role of these inflammatory cells in myocardial fibrogenesis was studied in the present work.
  
  
  METHODS
  The production and distribution of proteins that may be implicated in inflammation was examined by immunohistochemistry of sections of left ventricles from 1-month and 4-month renovascular hypertensive and age-matched control rats using antibodies against ICAM-1, LFA-1, TGF beta 1, PDGF-A, T and H kininogens, IgG, IgM, C3, and C5b-9. Infiltrating inflammatory cells were phenotyped by immunohistochemistry. The TGF beta 1 and PDGF-A mRNA levels were checked by RT-PCR.
  
  
  RESULTS
  Infiltrating cells were mainly T helper lymphocytes and macrophages, and there were more inflammatory cells in hypertensive rats than in control rats, localized especially around coronary arteries and in microscars. There were more ICAM-1 and LFA-1 in the ventricles of hypertensive than in control rats at 1 month, but the ICAM-1 expressions in hypertensive and control rats were similar at 4 months. TGF beta 1 and PDGF-A mRNA steady states increased in 4-month hypertensive rats, but there was no labeling for TGF beta or PDGF by immunohistochemistry. There was only faint labeling for T and H kininogens, and it was not increased in hypertensive rats. There were deposits of IgM and C5b-9 only in hypertensive rats.
  
  
  CONCLUSIONS
  Thus, inflammatory cells infiltrate the cardiac tissue of renovascular hypertensive rats as in the case of spontaneously hypertensive rats and these cells may use the ICAM-1/LFA-1 system to infiltrate, but neither TGF beta 1 and PDGF-A, nor the kininogen system seem to be associated with cardiac fibrogenesis. Otherwise, the complement system could act as arteriosclerotic and/or leukocyte mobilizing factors.
authors.affiliation: Unité 430 INSERM, Hôpital Broussais, Paris, France. nicolett@citi2.fr
authors.forename: A
authors.initials: A
authors.lastname: Nicoletti
authors.forename: C
authors.initials: C
authors.lastname: Mandet
authors.forename: M
authors.initials: M
authors.lastname: Challah
authors.forename: J
authors.initials: J
authors.lastname: Bariéty
authors.forename: J B
authors.initials: JB
authors.lastname: Michel
mesh_terms: D000818:Animals; D001483:Base Sequence; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D003176:Complement C3 / Q000378:metabolism; D015938:Complement Membrane Attack Complex / Q000378:metabolism; D017931:DNA Primers / Q000235:genetics; D019040:E-Selectin / Q000378:metabolism; D005355:Fibrosis; D006978:Hypertension, Renovascular / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D007075:Immunoglobulin M / Q000378:metabolism; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007704:Kininogens / Q000378:metabolism; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D008264:Macrophages / Q000473:pathology*; D008969:Molecular Sequence Data; D009206:Myocardium / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D010982:Platelet-Derived Growth Factor / Q000235:genetics / Q000378:metabolism; D016133:Polymerase Chain Reaction; D051381:Rats; D017208:Rats, Wistar; D006377:T-Lymphocytes, Helper-Inducer / Q000473:pathology*; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism
chemical_list: D015815:Cell Adhesion Molecules; D003176:Complement C3; D015938:Complement Membrane Attack Complex; D017931:DNA Primers; D019040:E-Selectin; D007075:Immunoglobulin M; D007704:Kininogens; D016169:Lymphocyte Function-Associated Antigen-1; D010982:Platelet-Derived Growth Factor; D016212:Transforming Growth Factor beta; D018799:Intercellular Adhesion Molecule-1