Expression of ADAMTS-2, -3, -13, and -14 in culprit coronary lesions in patients with acute myocardial infarction or stable angina.
ADAMTS (a disintegrin and metalloproteinase with thrombospondin type 1 motifs) proteases are emerging as key participants in the pathogenesis of vascular diseases. We studied the expression of ADAMTS-2, -3, -4 and -14 in the culprit plaques from patients presenting with acute myocardial infarction (AMI) versus stable angina. Tissue samples were gathered from 52 patients with AMI (n = 35) or stable angina (n = 17) who underwent directional coronary atherectomy. The specimens were stained with hematoxylin-eosin and analyzed immunohistochemically using antibodies specific to ADAMTS-2, -3, -13 and -14, and markers for endothelial cells, macrophages, and smooth muscle cells. Baseline characteristics of the groups were mostly similar. The proportion of smooth muscle α-actin-immunopositive area was smaller in the AMI group than in the stable angina group, but the areas immunopositive for CD31 or CD68 were higher in the AMI group. The relative areas immunopositive for ADAMTS-2, -3, and -13 in AMI were significantly larger than those in stable angina. However, the proportion of areas immunopositive for ADAMTS-14 did not differ between the two groups. Areas that stained for ADAMTS-2, -3, -13, and -14 largely overlapped with those positive for CD31 or CD68. The areas immunopositive for ADAMTS proteases were significantly correlated with CD31- or CD68-immunostained areas. In conclusions, ADAMTS-2, -3, and -13 expression, but not that of ADAMTS-14, are increased in plaques causing AMI compared those associated with stable angina. These results support a role for these enzymes in the pathogenesis of AMI.
Department of Medicine, University of Ulsan, Seoul, Korea.
Cheol Whan
CW
Lee
Ilseon
I
Hwang
Chan-Sik
CS
Park
Hyangsin
H
Lee
Duk-Woo
DW
Park
Su-Jin
SJ
Kang
Seung-Whan
SW
Lee
Young-Hak
YH
Kim
Seong-Wook
SW
Park
Seung-Jung
SJ
Park
D051722:ADAM Proteins / Q000096:biosynthesis*; D000071096:ADAMTS Proteins; D000071120:ADAMTS13 Protein; D000071121:ADAMTS4 Protein; D000199:Actins / Q000378:metabolism; D000368:Aged; D060050:Angina, Stable / Q000201:enzymology* / Q000473:pathology; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006801:Humans; D008297:Male; D008875:Middle Aged; D009124:Muscle Proteins / Q000096:biosynthesis*; D009203:Myocardial Infarction / Q000201:enzymology* / Q000473:pathology; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D011348:Procollagen N-Endopeptidase / Q000096:biosynthesis*; D000097382:CD68 Molecule
D051722:ADAM Proteins; D000071096:ADAMTS Proteins; D000071120:ADAMTS13 Protein; D000071121:ADAMTS4 Protein; D000199:Actins; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D009124:Muscle Proteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D011348:Procollagen N-Endopeptidase; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C447060:ADAMTS14 protein, human; C434951:ADAMTS3 protein, human; C000609307:ADAMTS2 protein, human; C099604:ADAMTS13 protein, human