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ENDOTHELIN-1 INVOLVED IN INFLAMMATORY RESPONSE IN
ATHEROSCLEROSIS: EVIDENCE OF ITS SWITCHING IN
CYTOKINES AND SOLUBLE CELL ADHESION MOLECULES
PROINFLAMMATORY PROGRAMME
A.I. Teplyakov
Research Institute for Ecopathology and Occupational Disease,
Mogilev, Belarus
A goal of present paper was the comparative analysis of possible ET-1
switching in pro- and antiinflammatory cytokines program and adhesive
molecules cascade in atherosclerosis. We studied samples of venous blood
of 29 patients, suffering from coronary and cerebral atherosclerosis. The
original research technique was developed. The baseline ET-1 level, sCAM:
P-, E-selectins, ICAM-1, VCAM-1 ('R&D', UK), Il-1a, IL-1b, IL-6, IL-8
and IL-10 (Immunotech, Prague) were detected and their changes in
response to coagulation and fibrinolysis (incubation of clot 6 hrs at 37 C)
and to standartized viscosimetric flow using rotational viscosimeter (shear
rate 100 -1/sec, 60 sec at 37 C, samples incubation 6 hrs also) were
measured by ELISA kits. ET-1 level was increased in both probes and after
rheologic test in two times by uncertain clear releasing mechanism. The
increased levels of IL-1b, IL-6, sP-, sE-selectins, sICAM-1 and sVCAM-1
were found even without functional probes in patients, suffering from
atherosclerosis. Theremore, the levels of IL-1a, IL-1b, IL-6, IL-8, IL-10 (but
not ICAM-1 and VCAM-1) dramatically increased after both tests, whereas
after rheologic test the P- and E-selection levels were statistically significant
decreased. The hard correlation between ET-1 and E-selectin levels in both
tests were detected (r=-0.90 and -0.89, p<0.001). By our results it may
hypothesize that multiple cell-cell mechanisms were switched on (Et-1
releasing and E-selectin reinternalisation? - this requests additional proof).
The Et-1 after both (coagulation and rheologic) tests was close correlated to
initial IL-1b level (r=0.61 and 0.69, p<0.05). By obtained results it may
speculate that the ET-1 is participating in realisation of cytokines- and
sCAM-induced proinflammatory response at atherosclerosis. The ET-1
antagonist may by useful in prevention of atherosclerosis progression and
complication.