Clinical Significance of Neutrophil Adhesion Molecules Expression after Coronary Angioplasty on the Development of Restenosis

Teruo Inoue; Yoshihiko Sakai; Tsuneo Fujito; Kazuhiro Hoshi; Terumi Hayashi; Kan Takayanagi; Shigenori Morooka

doi:10.1055/s-0037-1614219

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1998; 79(01): 54-58
DOI: 10.1055/s-0037-1614219

Review Article

Schattauer GmbH

Clinical Significance of Neutrophil Adhesion Molecules Expression after Coronary Angioplasty on the Development of Restenosis

Teruo Inoue

From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

,

Yoshihiko Sakai

From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

,

Tsuneo Fujito

From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

,

Kazuhiro Hoshi

From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

,

Terumi Hayashi

From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

,

Kan Takayanagi

From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

,

Shigenori Morooka

From the Department of Cardiology, Koshigaya Hospital, Dokkyo University School of Medicine, Saitama, Japan

› Author Affiliations

Abstract

Summary

To investigate the neutrophil activation process following percutaneous transluminal coronary angioplasty (PTCA), we examined the expressions of Mac-1 (CD11b/CD18), L-selectin (CD62L), and sialyl-Lewis^X (SLX) on the surface of neutrophils after the PTCA procedure, by flow cytometric analysis. Twenty-nine patients with single vessel coronary artery disease of the left anterior descending artery who underwent elective PTCA were enrolled. In the 17 patients without restenosis at the follow-up angiography, the mean channel fluorescence intensity (MFI) for CD18, CD62L and SLX did not change after PTCA. Only the CD11b level was increased at 48 h after the PTCA. In the remaining 12 patients who developed restenosis, the MFI values for CD18 and CD11b were increased at 24 h and 48 h after the PTCA. The MFI value for CD62L was decreased and that for SLX was increased at 48 h after the PTCA. These changes were more prominent in the coronary sinus blood samples than in those of the peripheral blood samples.

Our data indicate the down-regulation of L-selectin, probably by shedding, as well as the up-regulations of Mac-1 and sialyl-Lewis^X, especially in patients with restenosis. It is suggested that neutrophil activation by an interaction between the selectin family and carbohydrate ligands after PTCA may play a role in the development of restenosis, as does the integrin family.

Full Text

References

References
1 De Servi S, Mazzone A, Ricevuti G, Fioravanti A, Bramucci E, Angoli L, Ghio S, Specchia G. Granulocyte activation after coronary angioplasty in human. Circulation 1990; 82: 140-6.
2 Prescott MF, McBride CK, Court M. Development of intimal lesions after leukocyte migration into the vascular wall. Am J Pathol 1989; 135: 835-46.
3 Detmers PA, Wright SD. Adhesion-promoting receptors on leukocytes. Curr Opin Immunol 1988; 1: 10-5.
4 Arnaout NA, Lanier LL, Faller DV. Relative contribution of the leukocyte molecules Mo1, LFA-1, and p150,95 (Lew M5) in adhesion of granulocytes and monocytes to vascular endothelium is tissue- and stimulus-specific. J Cell Physiol 1988; 137: 305-9.
5 Freuyer DR, Morganroth ML, Todd RF. Surface Mo1 (CD11b/CD18) glycoprotein is up-modulated by neutrophils recruited to sites of inflammation in vivo. Inflammation 1989; 13: 495-505.
6 Butcher EC. Leukocyte-endothelial cell recognition: three (or more) steps to specificity and diversity. Cell 1991; 67: 1033-6.
7 Phillips ML, Nudelman E, Gaeta FCA, Perez M, Singhal AK, Hakomori S, Paulson JC. ELAM-1 mediates cell adhesion by recognition of a carbohydrate ligand, sialyl-LeX. Science 1990; 250: 1130-2.
8 The National Committee for Clinical Laboratory Standards. Clinical applications of flow cytometry: quality assurance and immunophenotyping of peripheral blood lymphocytes. NCCLS 1992; 12: 1-76.
9 Stephen HI, Ritterhaus CW, Hearley KW, Struzziero CC, Hoffman RA, Hansen PW. Rapid enumeration of T lymphocytes by a flow-cytometric immunofluorescence method. Clin Chem 1982; 28: 1905-9.
10 Wells DA, Daigneault-Creech CA, Simrell CR. Effect of iron status on reticulocyte mean channel fluorescence. Am J Clin Pathol 1992; 97: 130-4.
11 Holmes DR, Vlietstra RE, Smith HC, Vetrovec GW, Kent KM, Cowley MJ, Faxon DP, Gruenzig AR, Kelsey SF, Detre KM, Van Raden M, Mock MB. Restenosis after percutaneous transluminal coronary angioplasty (PTCA): a report from the PTCA registry of the National Heart, Lung, and Blood Institute. Am J Cardiol 1984; 53: 77C-81C.
12 Serruys PW, Luijten HE, Beatt KJ, Geusken R, de Feyter PJ, van den Brand M, Reiber JHC, ten Katen HJ, van Es GA, Hugenholtz PG. Incidence of restenosis after successful coronary angioplasty: a time-related phenomenon: a quantitative angiographic study in 342 consecutive patients at 1, 2, 3, and 4 months. Circulation 1988; 77: 361-71.
13 Nobuyoshi M, Kimura T, Nosaka H, Mioka S, Ueno K, Yokoi H, Hamasaki N, Horiuchi H, Ohishi H. Restenosis after successful percutaneous transluminal coronary angioplasty: serial angiographic follow-up of 229 patients. J Am Coll Cardiol 1988; 12: 616-23.
14 Calif RN, Fortin DF, Frid DJ, Harlan WR III, Ohman EM, Bengtson JR, Nelson CL, Tcheng JE, Mark DB, Stack RS. Restenosis after coronary angioplasty: an overview. J Am Coll Cardiol 1991; 17: 2B-13B.
15 Clowes AW, Reidy MA, Clowes MM. Mechanism of stenosis after arterial injury. Lab Invest 1983; 49: 208-15.
16 Clowes AW, Reidy MA, Clowes MM. Kinetics of cellular proliferation after arterial injury. Lab Invest 1983; 49: 327-33.
17 Waller BF, Gorfinkel HJ, Rogers FJ, Kent KM, Roberts WC. Early and late morphologic changes in major epicardial coronary arteries after percutaneous transluminal coronary angioplasty. Am J Cardiol 1984; 53: 42C-7C.
18 Forrester JS, Fishbein M, Helfant R, Fagin J. A paradigm for restenosis based on cell biology: clues for the development of new preventive therapies. J Am Coll Cardiol 1991; 17: 758-69.
19 Leibovich SJ, Ross R. A macrophage-dependent factor that stimulates the proliferation of fibroblasts in vivo. Am J Pathol 1976; 84: 501-13.
20 Ross R, Raines EW, Bowen-Pope DF. The biology of platelet-derived growth factor. Cell 1986; 46: 155-69.
21 Liw MW, Roubin GS, King SB III. Restenosis after coronary angioplasty: potential biologic determinants and role of intimal hyperplasia. Circulation 1989; 79: 1374-87.
22 Moyer CF, Sajuthi D, Tulli H, William JK. Synthesis of IL-1 arupha and IL-1 beta by arterial cells in atherosclerosis. Am J Pathol 1991; 138: 951-60.
23 Barath P, Fishbein MC, Cao J, Berenson J, Helfant RH, Forrester JS. Detection and localization of tumor necrosis factor in human atheroma. Am J Cardiol 1990; 65: 297-302.
24 Springer TA. Adhesion receptors in immune system. Nature 1990; 346: 425-34.
25 Sanchez-Madrid F, Nagy JA, Robbins E, Simon P, Springer TA. A human leukocyte differentiation antigen family with distinct a-subunits and a common b-subunit: the leukocyte function-associated antigen (LFA-1), the C3bi complement receptor (OKM1/Mac-1), and the p150,95 molecules. J Exp Med 1983; 158: 1785-803.
26 Kishimoto TK, O’Connor K, Lee A, Roberts TM, Springer TA. Cloning of the beta subunit of the leukocyte adhesion proteins: homology to an extracellular matrix receptor defines a novel supergene family. Cell 1987; 48: 681-90.
27 Patarroyo M, Prieto J, Rincon J, Timonen T, Lundberg C, Lindbom L, Asjo B, Gahmberg CG. Leukocyte-cell adhesion: a molecular process fundamental in lenkocyte physiology. Immunol Rev 1990; 14: 67-108.
28 Ikeda H, Nakayama H, Oda T, Kuwano K, Yamada A, Ueno T, Yoh M, Hiyamuta K, Koga Y, Toshima H. Neutrophil activation after percutaneous transluminal coronary angioplasty. Am Heart J 1994; 128: 1091-8.
29 Newmann FJ, Ott I, Gawaz M, Puchner G, Schömic A. Neutrophil and platelet activation at balloon-injured coronary artery plaque in patients undergoing angioplasty. J Am Coll Cardiol 1996; 27: 819-24.
30 Inoue T, Sakai Y, Morooka S, Hayashi T, Takayanagi K, Takabatake Y. Expression of polymorphonuclear leukocyte adhesion molecules and its clinical significance in patients treated with percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1996; 28: 1127-33.
31 Stenberg PE, McEver RP, Shuman MA, Jaques YV, Bainton DF. A platelet alpha-granule membrane protein (GMP-140) is expressed on the plasma membrane after activation. J Cell Biol 1985; 101: 880-6.
32 Handa K, Nudelman ED, Stroud MR, Shiozawa T, Hakomori S. Selectin GMP-140 (CD62; PADGEM) binds to sialosyl-Lea and sialosyl-Lex, and sulfate glycans modulate this binding. Biochem Biophis Res Commun 1991; 181: 1223-30.
33 Lasky LA, Singer MS, Dowbenko D, Imai Y, Henzel WJ, Grimley C, Fennie C, Gillett N, Watson SR, Rosen SD. An endothelial ligand for L-selectin is a novel mucin-like molecule. Cell 1992; 69: 927-38.
34 Baumhueter S, Singer MS, Henzel W, Hemmerich S, Renz M, Rosen SD, Lasky LA. Binding of L-selectin to vascular sialomucin CD34. Science 1993; 262: 436-8.
35 Kishimoto TK, Jutila MA, Berg EL, Bucher EC. Neutrophil Mac-1 and MEL-14 adhesion protein inversely regulated by chemotactic factors. Science 1989; 245: 1238-41.
36 Picker LJ, Warnock RA, Burns AR, Doerschuk CM, Berg EL, Butcher EC. The neutrophil selectin LECAM-1 presents carbohydrate ligands to the vascular selectins ELAM-1 and GMP-140. Cell 1991; 66: 921-33.
37 Lorant DE, McEver RP, McIntyre TM, Moore KL, Prescott SM, Zimmerman GA. Activation of polymorphonuclear leukocytes reduces their adhesion to P-selectin and causes redistribution of ligands for P-selectin on their surfaces. J Clin Invest 1995; 96: 171-82.