Antiphospholipid Antibodies Activate Vascular Endothelial Cells

Lupus ◽  
1996 ◽  
Vol 5 (5) ◽  
pp. 440-441 ◽  
Author(s):  
R Simantov ◽  
SK Lo ◽  
A Gharavi ◽  
LR Sammaritano ◽  
JE Salmon ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Antiphospholipid Antibodies ◽  
Vascular Endothelial Cells ◽  
Leukocyte Adhesion ◽  
Fetal Loss ◽  
Endothelial Activation ◽  
Vascular Endothelial ◽  
Endothelial Surface ◽  
Endotoxin Contamination ◽  
Leukocyte Adhesion Molecules

Antiphospholipid antibodies (aPL) are associated with a syndrome of arterial and venous thrombosis and recurrent fetal loss. We have shown that IgG purified from patients with aPL activate vascular endothelial cells (EC), converting the steady-state, non-thrombotic endothelial surface to a pro-thrombotic state. The aPL-activated EC are characterized by the expression of leukocyte adhesion molecules, including ICAM-1, VCAM, and E-selectin. EC activation is dependent upon the presence of β2-GP-I, a cofactor necessary for anticardiolipin reactivity. In addition, EC activation is not attributable to endotoxin contamination, Fc receptor interactions, or immune complexes, but rather is the result of the specific anticardiolipin reactivity of the IgG. Endothelial activation by aPL may be an important mechanism by which these antibodies cause a hypercoagulable state.

Diarylheptanoids suppress expression of leukocyte adhesion molecules on human vascular endothelial cells

2000 ◽  
Vol 404 (3) ◽  
pp. 375-385 ◽  
Author(s):  
Ryuta Yamazaki ◽  
Hiroshi Hatano ◽  
Ritsuo Aiyama ◽  
Takeshi Matsuzaki ◽  
Shusuke Hashimoto ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecules ◽  
Vascular Endothelial Cells ◽  
Leukocyte Adhesion ◽  
Vascular Endothelial ◽  
Leukocyte Adhesion Molecules

scholarly journals Activation of cultured vascular endothelial cells by antiphospholipid antibodies.

1995 ◽  
Vol 96 (5) ◽  
pp. 2211-2219 ◽  
Author(s):  
R Simantov ◽  
J M LaSala ◽  
S K Lo ◽  
A E Gharavi ◽  
L R Sammaritano ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Antiphospholipid Antibodies ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

scholarly journals Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity

2003 ◽  
Vol 83 (1) ◽  
pp. 59-115 ◽  
Author(s):  
Dirk L. Brutsaert
Keyword(s):  
Endothelial Cells ◽  
Signaling Pathways ◽  
Cardiac Failure ◽  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Endothelial Activation ◽  
Cardiac Metabolism ◽  
Vascular Endothelial ◽  
Adult Heart ◽  
Contractile Performance

Experimental work during the past 15 years has demonstrated that endothelial cells in the heart play an obligatory role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the molecular mechanisms and cellular signals governing this interaction, such as neuregulin, vascular endothelial growth factor, and angiopoietin, continue to maintain phenotype and survival of cardiomyocytes in the adult heart. Cardiac endothelial cells, like vascular endothelial cells, also express and release a variety of auto- and paracrine agents, such as nitric oxide, endothelin, prostaglandin I2, and angiotensin II, which directly influence cardiac metabolism, growth, contractile performance, and rhythmicity of the adult heart. The synthesis, secretion, and, most importantly, the activities of these endothelium-derived substances in the heart are closely linked, interrelated, and interactive. It may therefore be simplistic to try and define their properties independently from one another. Moreover, in relation specifically to the endocardial endothelium, an active transendothelial physicochemical gradient for various ions, or blood-heart barrier, has been demonstrated. Linkage of this blood-heart barrier to the various other endothelium-mediated signaling pathways or to the putative vascular endothelium-derived hyperpolarizing factors remains to be determined. At the early stages of cardiac failure, all major cardiovascular risk factors may cause cardiac endothelial activation as an adaptive response often followed by cardiac endothelial dysfunction. Because of the interdependency of all endothelial signaling pathways, activation or disturbance of any will necessarily affect the others leading to a disturbance of their normal balance, leading to further progression of cardiac failure.

Heparin-Like Glycosaminoglycans Inhibit Leukocyte Adhesion to Endotoxin-Activated Human Vascular Endothelial Cells under Nonstatic Conditions

1996 ◽  
Vol 28 (6) ◽  
pp. 428-435 ◽  
Author(s):  
N. Kitamura ◽  
M. Yamaguchi ◽  
K. Shimabukuro ◽  
M. Miyasaka ◽  
H. Nakano ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Leukocyte Adhesion ◽  
Vascular Endothelial
Sign in / Sign up

Export Citation Format

Share Document