Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We coimmobilized mast cell-derived heparin proteoglycans (HEP-PGs) of very high molecular weight (750 kDa) or unfractionated heparin (UFH) on coverslips together with collagen without altering the amount of immobilized collagen. Subsequently, platelet-collagen interactions were studied under both flowing and static conditions in D-phenylalanyl-L-prolyl-L-arginine chloromethyl ketone-anticoagulated blood and platelet-rich plasma (PRP), respectively. At a high shear rate (1600 1/s), the mean platelet deposition (PD) on collagen monomers was 7.5+/-6.1x10(6)/cm(2) (n=5). When the monomers were coimmobilized with UFH, PD was inhibited by 73% (2.0+/-1.2x10(6)/cm(2)), whereas HEP-PG completely blocked it (0. 42+/-0.38x10(6)/cm(2); P<0.05). Also, when collagen fibrils were used for coating, HEP-PG significantly inhibited PD. At a low shear rate (200 1/s) and under static conditions in PRP, the inhibitory effect of HEP-PG on PD was less marked. Inhibition of glycoprotein IIb/IIIa did not affect PD on coimmobilized HEP-PG in contrast to coimmobilized UFH or collagen alone. As a sign of inactivation, platelets adhering to the HEP-PG surface released considerably less beta-thromboglobulin than did those adhering to pure collagen. In summary, immobilized HEP-PG strongly inhibited PD on collagen by attenuating adhesion-induced platelet activation. The stronger effect on collagen monomers suggests the inhibition of glycoprotein Ia/IIa-mediated activation.
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PMID:Coimmobilized native macromolecular heparin proteoglycans strongly inhibit platelet-collagen interactions in flowing blood. 1107 64

Previously, during blood perfusion over collagen-coated surfaces; soluble or immobilized heparin proteoglycans (HEP-PG) have been shown to block thrombus growth. Our aim was to study the antithrombotic effect of locally applied unfractionated heparin (UFH, 1 mg/ml), or rat mast cell-derived HEP-PG (MW 750 kD, 10 microg/ml) compared with saline in early (10 min) and late (3 days) thrombus formation upon anastomosis of rat common femoral arteries. In both semiquantitative scanning electron microscopy (SEM) and quantitative platelet Indium 111-labeling HEP-PG inhibited thrombus growth in comparison with saline. At 10 min, the extent of thrombosis (scale 1-4) in SEM followed the order: saline (3.2+/-0.8) > UFH (2.8+/-1.0) > HEP-PG (1.8+/-0.8), and also Indium 111-positive platelets (10(6)) accumulated on the anastomosed vessel in the same order 14.2 +/-7.2, 10.3 +/-5.0, and 7.7 +/-3.1 (saline vs. HEP-PG, p = 0.03 and 0.05, respectively). At 3 days all HEP-PG-treated vessels remained patent with only small mural thrombi, whereas 2/7 saline- and 1/7 UFH-treated anastomoses occluded and showed more thrombosis overall. We conclude that locally administered HEP-PG inhibit arterial thrombus growth in anastomosed small-sized arteries and could prevent thrombotic complications in (micro)vascular surgery and arteriovenous shunts.
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PMID:Topically administered macromolecular heparin proteoglycans inhibit thrombus growth in microvascular anastomoses. 1185 84