OR.68. T-Cell Recognition of Vascular Smooth Muscle Cells (VSMC) in Patients with Unstable Atherosclerotic Plaque

2006 ◽  
Vol 119 ◽  
pp. S29
Author(s):  
Sergey Pryshchep ◽  
Jorg Goronzy ◽  
Cornelia Weyand
Keyword(s):  
Smooth Muscle ◽  
T Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Muscle Cells ◽  
Cell Recognition ◽  
T Cell Recognition ◽  
Unstable Atherosclerotic Plaque

scholarly journals TRAIL-expressing T cells induce apoptosis of vascular smooth muscle cells in the atherosclerotic plaque

2006 ◽  
Vol 203 (1) ◽  
pp. 239-250 ◽  
Author(s):  
Kayoko Sato ◽  
Alexander Niessner ◽  
Stephen L. Kopecky ◽  
Robert L. Frye ◽  
Jörg J. Goronzy ◽  
...  
Keyword(s):  
T Cells ◽  
Smooth Muscle ◽  
T Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Cd4 T Cells ◽  
Muscle Cells ◽  
Immunodeficient Mice

Acute coronary syndromes (ACS) are precipitated by a rupture of the atherosclerotic plaque, often at the site of T cell and macrophage infiltration. Here, we show that plaque-infiltrating CD4 T cells effectively kill vascular smooth muscle cells (VSMC). VSMCs sensitive to T cell–mediated killing express the death receptor DR5 (TNF-related apoptosis-inducing ligand [TRAIL] receptor 2), and anti-TRAIL and anti-DR5 antibodies block T cell–mediated apoptosis. CD4 T cells that express TRAIL upon stimulation are expanded in patients with ACS and more effectively induce VSMC apoptosis. Adoptive transfer of plaque-derived CD4 T cells into immunodeficient mice that are engrafted with human atherosclerotic plaque results in apoptosis of VSMCs, which was prevented by coadministration of anti-TRAIL antibody. These data identify that the death pathway is triggered by TRAIL-producing CD4 T cells as a direct mechanism of VSMC apoptosis, a process which may lead to plaque destabilization.

Processing of Chimeric Antisense Oligonucleotides by Human Vascular Smooth Muscle Cells and Human Atherosclerotic Plaque

Circulation ◽  
1996 ◽  
Vol 93 (4) ◽  
pp. 772-780 ◽  
Author(s):  
J. Geoffrey Pickering ◽  
Jeffrey M. Isner ◽  
Carol M. Ford ◽  
Lawrence Weir ◽  
Andrew Lazarovits ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Antisense Oligonucleotides ◽  
Muscle Cells ◽  
Human Atherosclerotic Plaque

Abstract 381: IL-19 Inhibits Atherosclerosis in LDLR-/- Mice by Modulating Cholesterol Uptake in Macrophages and Vascular Smooth Muscle Cells

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Khatuna Gabunia ◽  
Stephen P Ellison ◽  
James M Richards ◽  
Sheri E Kelemen ◽  
Michael V Autieri
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Atherosclerotic Plaque ◽  
Scavenger Receptor ◽  
Muscle Cells ◽  
Wild Type ◽  
Anti Inflammatory ◽  
M2 Phenotype

IL-19 is a recently described, putative anti-inflammatory cytokine which had previously been ascribed to be leukocyte specific. IL-19 is not detected in normal artery, but we detected IL-19 in multiple cell types in human atherosclerotic plaque suggesting a role for this interleukin in atherosclerosis. The purpose of this study was to determine whether administration of exogenous IL-19 could attenuate development of pre-formed atherosclerotic plaque, and to identify potential molecular mechanisms. LDLR-/- mice were fed high-fat diet for 12 weeks and then administered with 10ng/g/day IL-19 or PBS for an additional 8 weeks. En face analysis demonstrated that IL-19 could halt, but not reverse existing plaque (26.7+/-1.7%, 41.03+/-3.1%, 23.70+/-2.6% for baseline, PBS control, and IL-19-treated mice). Foam cell formation by macrophages and vascular smooth muscle cells (VSMC) is a hallmark event during atherosclerosis. Nothing has been reported regarding IL-19 effects on macrophage or VSMC lipid uptake; we therefore investigated whether IL-19 affects macrophage and VSMC cholesterol handling. Addition of IL-19 to wild-type bone marrow derived macrophages (BMDM) significantly promoted oxLDL uptake, conversely, BMDM from IL-19-/- mice had significantly less oxLDL uptake compared to wild-type BMDM. Addition of IL-19 to wild type BMDM significantly increased expression of scavenger receptor B1 (SR-B1), and decreased expression of inflammatory cytokines TNFα, IL-12b, MCP1. Interestingly, converse results were obtained with VSMC, as addition of IL-19 to wild-type VSMC decreased uptake of oxLDL ( p<0.05 ) and decreased expression of scavenger receptor CD36. VSMC isolated from IL-19-/- mice had increased uptake of oxLDL (p<0.0001). It is reported that M2 macrophages participate in plaque regression. IL-19 decreased IL-12b and significantly promoted the polarization of anti-inflammatory M2 phenotype in BMDM as evidenced by the increased expression of YM1 and IL-10 mRNA. These data demonstrate that IL-19 can inhibit progression of existing atherosclerotic plaque by modulating lipid metabolism in VSMC and macrophages and by promoting macrophage differentiation into an alternative, anti-inflammatory M2 phenotype.

scholarly journals Regulation of the Versican Promoter by the β-Catenin-T-cell Factor Complex in Vascular Smooth Muscle Cells

2005 ◽  
Vol 280 (13) ◽  
pp. 13019-13028 ◽  
Author(s):  
Maziar Rahmani ◽  
Jason T. Read ◽  
Jon M. Carthy ◽  
Paul C. McDonald ◽  
Brian W. Wong ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
T Cell ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
T Cell Factor
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