PMID- 10217652
OWN - NLM
STAT- MEDLINE
DCOM- 19990517
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 99
IP  - 16
DP  - 1999 Apr 27
TI  - Expression of cell adhesion molecules in dilated cardiomyopathy: evidence for 
      endothelial activation in inflammatory cardiomyopathy.
PG  - 2124-31
AB  - BACKGROUND: Dilated cardiomyopathy (DCM) is pathogenically linked to inflammatory 
      cardiomyopathy (InfCM), which is characterized by intramyocardial infiltration. 
      The transendothelial migration of immunocompetent cells is mediated by cell 
      adhesion molecules (CAMs). METHODS AND RESULTS: We investigated the expression 
      pattern of CAMs (immunoglobulin superfamily, 32 selectins, and beta1- and 
      beta2-integrins) in endomyocardial biopsies from DCM patients (n=152; left 
      ventricular ejection fraction <40%) using immunohistochemistry. Whereas few 
      specimens obtained at autopsy (controls; n=14) presented enhanced expression 
      regarding single endothelial CAMs (human leukocyte antigen [HLA] class I, 7%; 
      HLA-DR, 14%; CD29, 14%), none demonstrated concurrent abundance of >3 CAMs 
      (inflammatory endothelial activation), nor did any control tissue prove positive 
      for InfCM (>7.0 CD3+ lymphocytes per 1 mm2). In comparison, 64% (n=97) of the DCM 
      biopsies were evaluated positive for InfCM and 67% (n=101) for inflammatory 
      endothelial activation, respectively. Whereas expression of HLA class I, HLA-DR, 
      intercellular cell adhesion molecule-1, and CD29 was distributed homogeneously 
      within a patient's serial sections, immunoreactivity of vascular cell adhesion 
      molecule-1, lymphocyte function antigen-3, and the selectins was accentuated on 
      single vascular endothelia. Sixty-six percent of the DCM biopsies presented CD29 
      abundance also within the extracellular matrix and the sarcolemma. CD62P and 
      CD62E were present in 16% and 40% of the DCM patients, respectively. Endothelial 
      CAM representatives correlated with one another (P<0.05), except for CD62P with 
      HLA. Endothelial CAM expression correlated with intramyocardial infiltrates 
      phenotyped by the corresponding counterreceptors. CONCLUSIONS: Inflammatory 
      endothelial activation is present in 67% of DCM patients. Because CAM expression 
      correlates with the immunohistological diagnosis of InfCM and 
      counterreceptor-bearing intramyocardial infiltrates, evaluation of endothelial 
      CAMs might be of diagnostic significance in InfCM.
FAU - Noutsias, M
AU  - Noutsias M
AD  - Department of Cardiology, University Hospital Benjamin Franklin, Free University 
      of Berlin, Berlin, Germany. noutsias@zedat,fu-berlin.de
FAU - Seeberg, B
AU  - Seeberg B
FAU - Schultheiss, H P
AU  - Schultheiss HP
FAU - Kuhl, U
AU  - Kuhl U
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Antigens, CD)
RN  - 0 (CD18 Antigens)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Integrin beta1)
RN  - 0 (Selectins)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Antigens, CD/analysis
MH  - CD18 Antigens/analysis/biosynthesis
MH  - Cardiomyopathy, Dilated/*immunology/pathology
MH  - Cell Adhesion Molecules/analysis/*biosynthesis
MH  - Endothelium, Vascular/*immunology
MH  - Female
MH  - HLA-DR Antigens/analysis
MH  - Histocompatibility Antigens Class I/analysis
MH  - Humans
MH  - Inflammation
MH  - Integrin beta1/analysis/biosynthesis
MH  - Intercellular Adhesion Molecule-1/analysis/biosynthesis
MH  - Lymphocytes/immunology
MH  - Male
MH  - Middle Aged
MH  - Myocardium/*immunology/pathology
MH  - Selectins/analysis/biosynthesis
MH  - Vascular Cell Adhesion Molecule-1/analysis/biosynthesis
EDAT- 1999/04/27 00:00
MHDA- 1999/04/27 00:01
CRDT- 1999/04/27 00:00
PHST- 1999/04/27 00:00 [pubmed]
PHST- 1999/04/27 00:01 [medline]
PHST- 1999/04/27 00:00 [entrez]
AID - 10.1161/01.cir.99.16.2124 [doi]
PST - ppublish
SO  - Circulation. 1999 Apr 27;99(16):2124-31. doi: 10.1161/01.cir.99.16.2124.