Linked Life Data

9821816

Source:http://linkedlifedata.com/resource/pubmed/id/9821816

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1999-1-14
pubmed:abstractText
Extracellular-superoxide dismutase [EC 1.15.1.1] (EC-SOD) is a secretory glycoprotein with high affinity for heparin. This enzyme locates in blood vessel walls at a high enough level to suppress oxidative stress under normal conditions. EC-SOD is the major SOD isozyme in plasma, anchored to heparan sulfate proteoglycans in the glycocalyx of endothelial cell surfaces. Plasma EC-SOD is heterogeneous in heparin affinity and can be divided into five fractions, I to V, by heparin-HPLC. It has been suggested that EC-SOD form V is the primary form synthesized in the body and that EC-SOD forms with reduced heparin affinity are the result of proteolytic truncation of the C-terminal end of EC-SOD form V which is responsible for the binding with heparin. Recently, we reported that only plasma EC-SOD form V, with the highest heparin affinity, was increased by intravenous injection of heparin. The heparin affinity of plasma EC-SOD in patients with coronary atherosclerosis (CA+ patients) was compared in this study. The increase of plasma EC-SOD form V after heparin injection in CA+ patients was significantly less than that in subjects without evidence of stenosis in their major coronary arteries (CA- subjects). On the other hand, in CA+ patients, EC-SOD forms I to III, with low heparin affinity, were significantly increased compared to those in CA- subjects. EC-SOD in plasma apparently forms an equilibrium between the plasma phase and endothelial cell surface, and EC-SOD on the endothelial cell surface contributes to protecting the vessel wall against oxidative stress. These findings suggest that the quantitative and qualitative changes of EC-SOD, i.e., the decrease of bound EC-SOD on the endothelial cell surface, might suppress the defense systems against oxidative stress, which causes in part the development of coronary artery atherosclerosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0918-6158
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1090-3
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Changes in the heparin affinity of extracellular-superoxide dismutase in patients with coronary artery atherosclerosis.
pubmed:affiliation
Laboratory of Clinical Pharmaceutics, Gifu Pharmaceutical University, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't