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Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction
by
Bank, Sarbashri
, Sinha, A. K.
, Guha, Santanu
, Jana, Pradipta
, Maiti, Smarajit
in
13/1
/ 631/45/173
/ 692/308/2778
/ 82/29
/ 82/83
/ 9/25
/ Acute coronary syndromes
/ Adult
/ Affinity
/ Aspirin
/ Aspirin - pharmacology
/ Aspirin - therapeutic use
/ Binding sites
/ Blood platelets
/ Case-Control Studies
/ Coronary artery
/ Female
/ Heart attacks
/ Humanities and Social Sciences
/ Humans
/ Male
/ Middle Aged
/ multidisciplinary
/ Myocardial infarction
/ Myocardial Infarction - blood
/ Myocardial Infarction - drug therapy
/ Peptides - physiology
/ Platelet aggregation
/ Platelet Aggregation - drug effects
/ Platelet Aggregation Inhibitors - pharmacology
/ Platelet Aggregation Inhibitors - therapeutic use
/ Platelet-Rich Plasma - drug effects
/ Protein Binding
/ Protein Isoforms - physiology
/ Rupture
/ Salicylic acid
/ Science
2014
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Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction
by
Bank, Sarbashri
, Sinha, A. K.
, Guha, Santanu
, Jana, Pradipta
, Maiti, Smarajit
in
13/1
/ 631/45/173
/ 692/308/2778
/ 82/29
/ 82/83
/ 9/25
/ Acute coronary syndromes
/ Adult
/ Affinity
/ Aspirin
/ Aspirin - pharmacology
/ Aspirin - therapeutic use
/ Binding sites
/ Blood platelets
/ Case-Control Studies
/ Coronary artery
/ Female
/ Heart attacks
/ Humanities and Social Sciences
/ Humans
/ Male
/ Middle Aged
/ multidisciplinary
/ Myocardial infarction
/ Myocardial Infarction - blood
/ Myocardial Infarction - drug therapy
/ Peptides - physiology
/ Platelet aggregation
/ Platelet Aggregation - drug effects
/ Platelet Aggregation Inhibitors - pharmacology
/ Platelet Aggregation Inhibitors - therapeutic use
/ Platelet-Rich Plasma - drug effects
/ Protein Binding
/ Protein Isoforms - physiology
/ Rupture
/ Salicylic acid
/ Science
2014
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Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction
by
Bank, Sarbashri
, Sinha, A. K.
, Guha, Santanu
, Jana, Pradipta
, Maiti, Smarajit
in
13/1
/ 631/45/173
/ 692/308/2778
/ 82/29
/ 82/83
/ 9/25
/ Acute coronary syndromes
/ Adult
/ Affinity
/ Aspirin
/ Aspirin - pharmacology
/ Aspirin - therapeutic use
/ Binding sites
/ Blood platelets
/ Case-Control Studies
/ Coronary artery
/ Female
/ Heart attacks
/ Humanities and Social Sciences
/ Humans
/ Male
/ Middle Aged
/ multidisciplinary
/ Myocardial infarction
/ Myocardial Infarction - blood
/ Myocardial Infarction - drug therapy
/ Peptides - physiology
/ Platelet aggregation
/ Platelet Aggregation - drug effects
/ Platelet Aggregation Inhibitors - pharmacology
/ Platelet Aggregation Inhibitors - therapeutic use
/ Platelet-Rich Plasma - drug effects
/ Protein Binding
/ Protein Isoforms - physiology
/ Rupture
/ Salicylic acid
/ Science
2014
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Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction
Journal Article
Dermcidin isoform-2 induced nullification of the effect of acetyl salicylic acid in platelet aggregation in acute myocardial infarction
2014
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Overview
The aggregation of platelets on the plaque rupture site on the coronary artery is reported to cause both acute coronary syndromes (ACS) and acute myocardial infarction (AMI). While the inhibition of platelet aggregation by acetyl salicylic acid was reported to produce beneficial effects in ACS, it failed to do in AMI. The concentration of a stress induced protein (dermcidin isoform-2) was much higher in AMI than that in ACS. Incubation of normal platelet rich plasma (PRP) with dermcidin showed one high affinity (K
d
= 40 nM) and one low affinity binding sites (K
d
= 333 nM). When normal PRP was incubated with 0.4 μM dermcidin, the platelets became resistant to the inhibitory effect of aspirin similar to that in the case of AMI. Incubation of PRP from AMI with dermcidin antibody restored the sensitivity of the platelets to the aspirin effect. Incubation of AMI PRP pretreated with 15 μM aspirin, a stimulator of the NO synthesis, resulted in the increased production of NO in the platelets that removed the bound dermcidin by 40% from the high affinity binding sites of AMI platelets. When the same AMI PRP was retreated with 10 μM aspirin, the aggregation of platelets was completely inhibited by NO synthesis.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 82/29
/ 82/83
/ 9/25
/ Adult
/ Affinity
/ Aspirin
/ Female
/ Humanities and Social Sciences
/ Humans
/ Male
/ Myocardial Infarction - blood
/ Myocardial Infarction - drug therapy
/ Platelet Aggregation - drug effects
/ Platelet Aggregation Inhibitors - pharmacology
/ Platelet Aggregation Inhibitors - therapeutic use
/ Platelet-Rich Plasma - drug effects
/ Protein Isoforms - physiology
/ Rupture
/ Science
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