ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker
Experimental and clinical data indicate that the initiation and progress of atherosclerosis and its clinical manifestations are first caused by circulating apoB-100 lipoproteins that enter and are retained in the arterial intima. Extracellular sulfated proteoglycans (PGs) of the intima are the reten...
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doaj-bacd51f6e33e42bfb4a70e8ac63aaed62020-11-24T23:22:41ZengMDPI AGJournal of Cardiovascular Development and Disease2308-34252018-07-01533610.3390/jcdd5030036jcdd5030036ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease BiomarkerEva Hurt-Camejo0Germán Camejo1Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institutet, 141 86 Stockholm, SwedenDivision of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institutet, 141 86 Stockholm, SwedenExperimental and clinical data indicate that the initiation and progress of atherosclerosis and its clinical manifestations are first caused by circulating apoB-100 lipoproteins that enter and are retained in the arterial intima. Extracellular sulfated proteoglycans (PGs) of the intima are the retention agents. The PGs also initiate physical and biochemical lipoprotein degradation with the production of bioactive, lipid products that trigger an inflammatory response that leads to atherosclerosis. There are many simple methods for measuring abnormalities of circulating lipoproteins and their relation to atherosclerotic cardiovascular disease (ACVD). However, limited research aims to evaluate procedures that could report quantitatively about the contribution of the interaction of apoB-100 lipoprotein-arterial intima PGs to clinical manifestation of ACVD. In the present review we discuss observations indicating that simple ex vivo evaluation of the affinity of apoB-100 lipoproteins for arterial PGs and glycosaminoglycans (GAGs) can give an indication of its association with clinical manifestations of atherosclerosis. In addition, we discuss molecular and cellular aspects of the apoB-100 lipoproteins association with arterial PGs that are related to atherogenesis and that support the experimental framework behind the current “Response-to-Retention” hypothesis of atherosclerosis.http://www.mdpi.com/2308-3425/5/3/36apoB-100 lipoproteinsproteoglycansinteractionatherosclerosis |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Eva Hurt-Camejo Germán Camejo |
spellingShingle |
Eva Hurt-Camejo Germán Camejo ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker Journal of Cardiovascular Development and Disease apoB-100 lipoproteins proteoglycans interaction atherosclerosis |
author_facet |
Eva Hurt-Camejo Germán Camejo |
author_sort |
Eva Hurt-Camejo |
title |
ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker |
title_short |
ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker |
title_full |
ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker |
title_fullStr |
ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker |
title_full_unstemmed |
ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker |
title_sort |
apob-100 lipoprotein complex formation with intima proteoglycans as a cause of atherosclerosis and its possible ex vivo evaluation as a disease biomarker |
publisher |
MDPI AG |
series |
Journal of Cardiovascular Development and Disease |
issn |
2308-3425 |
publishDate |
2018-07-01 |
description |
Experimental and clinical data indicate that the initiation and progress of atherosclerosis and its clinical manifestations are first caused by circulating apoB-100 lipoproteins that enter and are retained in the arterial intima. Extracellular sulfated proteoglycans (PGs) of the intima are the retention agents. The PGs also initiate physical and biochemical lipoprotein degradation with the production of bioactive, lipid products that trigger an inflammatory response that leads to atherosclerosis. There are many simple methods for measuring abnormalities of circulating lipoproteins and their relation to atherosclerotic cardiovascular disease (ACVD). However, limited research aims to evaluate procedures that could report quantitatively about the contribution of the interaction of apoB-100 lipoprotein-arterial intima PGs to clinical manifestation of ACVD. In the present review we discuss observations indicating that simple ex vivo evaluation of the affinity of apoB-100 lipoproteins for arterial PGs and glycosaminoglycans (GAGs) can give an indication of its association with clinical manifestations of atherosclerosis. In addition, we discuss molecular and cellular aspects of the apoB-100 lipoproteins association with arterial PGs that are related to atherogenesis and that support the experimental framework behind the current “Response-to-Retention” hypothesis of atherosclerosis. |
topic |
apoB-100 lipoproteins proteoglycans interaction atherosclerosis |
url |
http://www.mdpi.com/2308-3425/5/3/36 |
work_keys_str_mv |
AT evahurtcamejo apob100lipoproteincomplexformationwithintimaproteoglycansasacauseofatherosclerosisanditspossibleexvivoevaluationasadiseasebiomarker AT germancamejo apob100lipoproteincomplexformationwithintimaproteoglycansasacauseofatherosclerosisanditspossibleexvivoevaluationasadiseasebiomarker |
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