Inhibition of rupture of established atherosclerotic plaques by treatment with apolipoprotein A-I
- Publication Type:
- Journal Article
- Citation:
- Cardiovascular Research, 2011, 91 (1), pp. 37 - 44
- Issue Date:
- 2011-07-01
Closed Access
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2011000544OK.pdf | 289.15 kB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Reimers, GJ | en_US |
dc.contributor.author | Jackson, CL | en_US |
dc.contributor.author | Rickards, J | en_US |
dc.contributor.author | Chan, PY | en_US |
dc.contributor.author | Cohn, JS | en_US |
dc.contributor.author | Rye, KA | en_US |
dc.contributor.author | Barter, PJ | en_US |
dc.contributor.author |
Rodgers, KJ https://orcid.org/0000-0002-3627-9651 |
en_US |
dc.date.issued | 2011-07-01 | en_US |
dc.identifier.citation | Cardiovascular Research, 2011, 91 (1), pp. 37 - 44 | en_US |
dc.identifier.issn | 0008-6363 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/18611 | |
dc.description.abstract | AimsPlasma concentrations of high-density lipoprotein (HDL)-cholesterol correlate inversely with the incidence of myocardial infarction in humans. We investigated the effect of treatment with human apolipoprotein A-I (apoA-I), the principal protein of HDL, on plaque disruption in an animal model.Methods and resultsSeventy apolipoprotein E knockout mice were induced to develop atherosclerotic lesions in the brachiocephalic artery by feeding a high-fat diet for 9 weeks. Mice then received twice-weekly treatment with human apoA-I (8 mg/kg) or vehicle, for 2 weeks. The incidence of acute plaque disruption was reduced by 65 in mice receiving apoA-I (P < 0.01). Plaques in treated mice had a more stable phenotype, with an increase in smooth muscle cell (SMC): macrophage ratio (P 0.05), principally the consequence of an increase in the number of SMC in plaques. In the fibrous cap, there were reductions in matrix metalloproteinase-13 (-69, P < 0.0001) and S100A4, a marker of SMC de-differentiation (-60, P < 0.0001). These results indicate that 2 weeks of treatment with small amounts of human apoA-I produces more stable plaques in a mouse model.ConclusionTreatment with apoA-I has the potential to stabilize plaques and prevent plaque rupture in humans. © 2011 The Author. | en_US |
dc.relation.ispartof | Cardiovascular Research | en_US |
dc.relation.isbasedon | 10.1093/cvr/cvr057 | en_US |
dc.subject.classification | Cardiovascular System & Hematology | en_US |
dc.subject.mesh | Muscle, Smooth, Vascular | en_US |
dc.subject.mesh | Brachiocephalic Trunk | en_US |
dc.subject.mesh | Macrophages | en_US |
dc.subject.mesh | Myocytes, Smooth Muscle | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Mice, Inbred C57BL | en_US |
dc.subject.mesh | Mice, Knockout | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Mice | en_US |
dc.subject.mesh | Disease Models, Animal | en_US |
dc.subject.mesh | Rupture, Spontaneous | en_US |
dc.subject.mesh | Fibrosis | en_US |
dc.subject.mesh | Collagen | en_US |
dc.subject.mesh | Apolipoprotein A-I | en_US |
dc.subject.mesh | Apolipoproteins E | en_US |
dc.subject.mesh | S100 Proteins | en_US |
dc.subject.mesh | Inflammation Mediators | en_US |
dc.subject.mesh | Cardiovascular Agents | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Atherosclerosis | en_US |
dc.subject.mesh | Cholesterol, HDL | en_US |
dc.subject.mesh | Matrix Metalloproteinase 13 | en_US |
dc.subject.mesh | Cell Dedifferentiation | en_US |
dc.subject.mesh | Plaque, Atherosclerotic | en_US |
dc.subject.mesh | S100 Calcium-Binding Protein A4 | en_US |
dc.title | Inhibition of rupture of established atherosclerotic plaques by treatment with apolipoprotein A-I | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 1 | en_US |
utslib.citation.volume | 91 | en_US |
utslib.for | 0601 Biochemistry and Cell Biology | en_US |
utslib.for | 1102 Cardiorespiratory Medicine and Haematology | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
pubs.organisational-group | /University of Technology Sydney/Strength - CHT - Health Technologies | |
utslib.copyright.status | closed_access | |
pubs.issue | 1 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 91 | en_US |
Abstract:
AimsPlasma concentrations of high-density lipoprotein (HDL)-cholesterol correlate inversely with the incidence of myocardial infarction in humans. We investigated the effect of treatment with human apolipoprotein A-I (apoA-I), the principal protein of HDL, on plaque disruption in an animal model.Methods and resultsSeventy apolipoprotein E knockout mice were induced to develop atherosclerotic lesions in the brachiocephalic artery by feeding a high-fat diet for 9 weeks. Mice then received twice-weekly treatment with human apoA-I (8 mg/kg) or vehicle, for 2 weeks. The incidence of acute plaque disruption was reduced by 65 in mice receiving apoA-I (P < 0.01). Plaques in treated mice had a more stable phenotype, with an increase in smooth muscle cell (SMC): macrophage ratio (P 0.05), principally the consequence of an increase in the number of SMC in plaques. In the fibrous cap, there were reductions in matrix metalloproteinase-13 (-69, P < 0.0001) and S100A4, a marker of SMC de-differentiation (-60, P < 0.0001). These results indicate that 2 weeks of treatment with small amounts of human apoA-I produces more stable plaques in a mouse model.ConclusionTreatment with apoA-I has the potential to stabilize plaques and prevent plaque rupture in humans. © 2011 The Author.
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