Monocyte chemotactic S19 ribosomal protein dimer in atherosclerotic vascular lesion.
To elucidate the molecular mechanism inducing monocyte/macrophage infiltration in the atherosclerotic lesion, we measured the monocyte chemotactic capacity in the extracts of aortic lesions. Five out of seven extracts exhibited significant chemotactic activities. Immunohistochemical examination with an anti-CD68 monoclonal antibody demonstrated that the five positive lesions possessed obvious monocyte/macrophage infiltrations at the intima, whereas the two negative lesions did so at significantly lower intensities. We subjected the chemotactic extracts to immunological analyses to identify the monocyte chemoattractant in them. The monocyte chemotactic capacities of all positive extracts were removed with anti-S19 ribosomal protein (RP S19) antibody beads and antimonocyte chemoattractant protein-1 (MCP-1) antibody beads. In three of the five extracts, the anti-RP S19 antibody beads were more effective than the anti-MCP-1 antibody beads for removal, while in the remaining two extracts, the opposite was observed. A combined immunoabsorption with these beads depleted the monocyte chemotactic capacity of a representative sample of each group. Consistently, the chemotactic capacity of an apparently RP S19 dimer-predominant extract was strongly inhibited by the presence of a C5a receptor antagonist. These results suggest that the RP S19 dimer and MCP-1 play a major role in the monocyte/macrophage infiltration of the atherosclerotic vascular lesion.
Shi
Lei
L
Department of Molecular Pathology, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University, 2-2-1 Honjo, Kumamoto, 860-0811, Japan.
Tsurusaki
Shigeyuki
S
Futa
Noriko
N
Sakamoto
Tamami
T
Matsuda
Tomoko
T
Nishino
Norikazu
N
Kunitomo
Ryuji
R
Kawasuji
Michio
M
Tokita
Kazutaka
K
Yamamoto
Tetsuro
T
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D000915:Antibody Affinity; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D002634:Chemotaxis, Leukocyte / Q000502:physiology*; D003324:Coronary Artery Disease / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007150:Immunohistochemistry; D008565:Membrane Proteins / Q000037:antagonists & inhibitors; D009000:Monocytes / Q000378:metabolism / Q000473:pathology; D010446:Peptide Fragments / Q000276:immunology / Q000378:metabolism*; D011817:Rabbits; D044087:Receptor, Anaphylatoxin C5a / Q000378:metabolism; D011951:Receptors, Complement / Q000037:antagonists & inhibitors; D012269:Ribosomal Proteins / Q000378:metabolism*; D000097382:CD68 Molecule
D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D018932:Chemokine CCL2; D008565:Membrane Proteins; D010446:Peptide Fragments; D044087:Receptor, Anaphylatoxin C5a; D011951:Receptors, Complement; D012269:Ribosomal Proteins; C488033:C5AR1 protein, human; C111835:CCL2 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C040343:ribosomal protein S19