19 research outputs found
The GPVI - Fc Fusion Protein Revacept Reduces Thrombus Formation and Improves Vascular Dysfunction in Atherosclerosis without Any Impact on Bleeding Times
Glycoprotein VI (GPVI) is a key platelet receptor which mediates plaque-induced platelet activation and consecutive atherothrombosis, but GPVI is also involved in platelet-mediated atheroprogression. Therefore, interference in GPVI-mediated platelet activation has the potential to combine short-term and long-term beneficial effects, specificity and safety especially regarding bleeding complications
Macroscopic and histological assessment of atherosclerosis in cholesterol-fed rabbits.
<p>(a) Plaque size [%] was determined in macroscopic en face preparations after sudan red staining of the common carotid arteries. The relative lesion area was expressed as percentage of the total vessel area of the common carotid artery. (b) Vessel wet weight to body weight ratio was determined. The mean ± SEM of 8 animals are shown. * indicates significant difference of p<0.05 versus cholesterol-fed atherosclerotic control rabbits.</p
Serum cholesterol levels of the Revacept group and the control group before, 4 and 8 weeks after feeding a high-cholesterol diet (means ± SEM).
<p>Serum cholesterol levels of the Revacept group and the control group before, 4 and 8 weeks after feeding a high-cholesterol diet (means ± SEM).</p
Pharmacokinetic profile of Revacept in rabbits (A) on the first day of dosing (after 4 weeks of high cholesterol feeding), (B) after the last dosing of the twice weekly dosing period four weeks later.
<p>The graphs show single animal and mean values of the Revacept group.</p
Effect of systemic delivery of increasing doses of Revacept in rabbits.
<p>Thrombus formation was induced by balloon vascular injury. The thrombus size was evaluated histologically post mortem and is expressed as % of the total vascular lesion area. The mean ± SD of n = 8 experiments per group are shown. * indicates significant difference of p<0.05, and ** of p<0.01, versus controls (as determined by ANOVA).</p
Representative images of plaque extensions in artery sections.
<p>LC: left carotid artery; RC: right carotid artery, Thor A: thoracic aorta, Abd A: abdominal aorta.</p
Representative images of thrombi in carotid artery preparations (en face).
<p>LC: left carotid artery; RC: right carotid artery.</p
Representative immuno-histological images of macrophage and T lymphocyte stains of carotid artery sections.
<p>Representative immuno-histological images of macrophage and T lymphocyte stains of carotid artery sections.</p
Study protocols of thrombus size detection after carotis artery lesion (upper panel), and of atherosclerosis in cholesterol-fed rabbits after eight weeks of drug administration (lower panel).
<p>Study protocols of thrombus size detection after carotis artery lesion (upper panel), and of atherosclerosis in cholesterol-fed rabbits after eight weeks of drug administration (lower panel).</p
The inflammation in the arterial wall was assessed by immune-histology in carotid artery sections of cholesterol fed rabbits.
<p>(a) The density of macrophages was determined using specific anti-RAM antibodies.(b) The density of T-lymphatic cells was determined with specific anti CD 4 antibodies. The mean ± SEM of 8 animals are shown.</p