Endothelin-1 involved in systemic cytokine network inflammatory response at atherosclerosis.
OBJECTIVE
Endothelin-1 (ET-1) switching in cytokines program and adhesive cascade at atherosclerosis.


OBJECTIVE
29 patients, suffering from atherosclerosis. The initial ET-1, sCAM: P-, E-selectins, ICAM-1, VCAM-1 levels and IL-1a, IL-1b, IL-6, IL-8 and IL-10 levels and their changes in response to high shear stress (shear rate 100/second, incubation for 6 hours at 37 degrees C) and blood coagulation (incubation at 37 degrees C for 6 hours also) were measured by ELISA kits.


RESULTS
ET-1 level was increased after both tests by unclear mechanisms of its releasing. The increased level of all researched molecules was detected without tests even. After shear stress the sP- and sE-selectins levels were significantly decreased, whereas their levels were strong correlated to ET-1.


CONCLUSIONS
We hypothesized that the multiple mechanisms of cell-cell communication were switched on (ET-1 releasing and selctin reinternalization). The ET-1 were closely correlated to proinflammatory cytokines. We postulate that the ET-1 is active participant in cytokine- and sCAM-induced inflammatory repsonse at atherosclerosis.
Teplyakov
Andrei I
AI
Research Institute for Ecopathology and Occupational Diseases, Mogilev, Belarus. teplyakov@mail.telecom.mogilev.by
D050197:Atherosclerosis / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D001777:Blood Coagulation; D015815:Cell Adhesion Molecules / Q000097:blood; D016207:Cytokines / Q000097:blood*; D019332:Endothelin-1 / Q000097:blood*; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000276:immunology / Q000378:metabolism*; D018836:Inflammation Mediators / Q000097:blood*; D013314:Stress, Mechanical; D015854:Up-Regulation
D015815:Cell Adhesion Molecules; D016207:Cytokines; D019332:Endothelin-1; D018836:Inflammation Mediators