Enhanced expression of haemoglobin scavenger receptor in accumulated macrophages of culprit lesions in acute coronary syndromes.
OBJECTIVE
Effective clearance of extracellular haemoglobin (Hb) is thought to limit systemic oxidative heme toxicity, which is presumed to contribute to the pathogenesis of plaque instability. We immunohistochemically examined the relationship between intraplaque haemorrhage, 4-HNE (4-hydroxy-2-nonenal), an index of lipid peroxidation, and the Hb scavenger receptor (CD163), using coronary atherectomy specimens from 74 patients with stable angina pectoris (SAP, n = 39) or unstable angina pectoris (UAP, n = 35).


RESULTS
Atherectomy samples were stained with antibodies against glycophorin A (a protein specific to erythrocyte membranes), CD31, 4-HNE, and CD163. Quantitative analysis demonstrated that glycophorin A-positive areas, 4-HNE-positive macrophage score, and CD163-positive macrophage score in UAP patients were significantly higher (glycophorin A, P < 0.0001; 4-HNE-positive macrophage score, P < 0.0001; CD163-positive macrophage score, P < 0.0005) than in SAP patients. The percentage of the glycophorin A-positive area showed a significant positive correlation with the number of CD31-positive microvessels and the 4-HNE-positive macrophage score (microvessels, R = 0.59, P < 0.0001; 4-HNE, R = 0.59, P < 0.0001). Moreover, the CD163-positive macrophage score was positively correlated with glycophorin A-positive area and the 4-HNE-positive macrophage score (glycophorin A, R = 0.58, P < 0.0001; 4-HNE, R = 0.53, P < 0.0001).


CONCLUSIONS
These findings suggest a positive association among intraplaque haemorrhage, enhanced expression of Hb scavenger receptor, and lipid peroxidation in human unstable plaques.
Yunoki
Kei
K
Department of Cardiology, Osaka City General Hospital, Osaka, Japan.
Naruko
Takahiko
T
Komatsu
Ryushi
R
Ehara
Shoichi
S
Shirai
Nobuyuki
N
Sugioka
Kenichi
K
Nakagawa
Masashi
M
Kitabayashi
Chizuko
C
Ikura
Yoshihiro
Y
Itoh
Akira
A
Kusano
Kengo
K
Ohe
Tohru
T
Haze
Kazuo
K
Becker
Anton E
AE
Ueda
Makiko
M
D054058:Acute Coronary Syndrome / Q000378:metabolism / Q000473:pathology*; D000368:Aged; D000447:Aldehydes / Q000378:metabolism*; D000787:Angina Pectoris / Q000473:pathology; D015703:Antigens, CD / Q000378:metabolism*; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology; D003432:Cross-Linking Reagents / Q000378:metabolism*; D005260:Female; D015870:Gene Expression; D006470:Hemorrhage / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011956:Receptors, Cell Surface / Q000378:metabolism*; D051116:Receptors, Scavenger / Q000378:metabolism*; D000098902:CD163 Antigen
D000447:Aldehydes; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D003432:Cross-Linking Reagents; D011956:Receptors, Cell Surface; D051116:Receptors, Scavenger; C027576:4-hydroxy-2-nonenal