Nobuhisa Hagiwara
Department Other, Other Position |
|
Article types | Original article |
Language | English |
Peer review | Peer reviewed |
Title | P-Selectin Glycoprotein Ligand-1 (PSGL-1) Expressing CD4 T Cells Contribute Plaque Instability in Acute Coronary Syndrome. |
Journal | Formal name:Circulation journal : official journal of the Japanese Circulation Society Abbreviation:Circ J ISSN code:1346-9843/1347-4820 |
Domestic / Foregin | Domestic |
Publisher | Japanese Circulation Society |
Volume, Issue, Page | 82(8),pp.2128-2135 |
Author and coauthor | KITAMURA Kazutaka†, SATO Kayoko*, SAWABE Motoji, YOSHIDA Masayuki, HAGIWARA Nobuhisa |
Authorship | Last author |
Publication date | 2018/07 |
Summary | Background: Adhesion molecules have essential roles in the development of atherosclerosis. We investigated whether P-selectin glycoprotein ligand-1 (PSGL-1)-expressing CD4 T cells contribute to plaque instability in acute coronary syndrome (ACS).
Methods and Results: We studied the adhesion molecules on CD4 T cells from consecutive patients with ACS treated with thrombus-aspirating device and compared them with healthy controls (n=48 each). Blood, thrombi, and plaque samples from the culprit coronary arteries were collected by thrombus aspiration performed during emergency coronary artery angiography. According to flow cytometry results, peripheral CD4 T cells from ACS patients strongly expressed PSGL-1 and integrin β2 (P<0.05 for both) more than those from controls; culprit coronary arteries contained an abundance of PSGL-1+ (P<0.001) but not integrin β2+CD4 T cells. In addition, immunohistochemical analysis of the thrombus-aspirating device samples revealed numerous PSGL-1+CD4 T cells in plaques from the culprit lesions. Results from the selectin-binding assay demonstrated that activated PSGL-1+CD4 T cells from ACS patients bound to P- or E-selectin after triggering the T-cell receptor, and adhered to endothelial cells under laminar flow conditions (P<0.05 and P<0.05, respectively), inducing their apoptosis (P<0.01) via activated caspase-3, which correlated with PSGL-1 expression (R=0.788, P=0.021) and was suppressed by application of a PSGL-1-specific antibody (P<0.05). Conclusions: PSGL-1 contributed to cytotoxic CD4 T cell homing to the culprit coronary artery and promoted plaque instability in ACS. |
DOI | 10.1253/circj.CJ-17-1270 |
PMID | 29962384 |