Cerebrovascular amyloid Angiopathy in bioengineered vessels is reduced by high-density lipoprotein particles enriched in Apolipoprotein E
Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood....
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| Published in | Molecular neurodegeneration Vol. 15; no. 1; pp. 23 - 21 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
BioMed Central
25.03.2020
BioMed Central Ltd BMC |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1750-1326 1750-1326 |
| DOI | 10.1186/s13024-020-00366-8 |
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| Abstract | Background
Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood.
Methods
Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces Aβ deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding.
Results
We demonstrate that HDL reduces vascular Aβ accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents Aβ-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering Aβ binding to collagen-I, ii) forming a complex with Aβ that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating Aβ uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE.
Conclusion
The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to Aβ and shed new light on a potential role of peripherally-acting apoE in AD. |
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| AbstractList | Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid (A[beta]) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood. Methods Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces A[beta] deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding. Results We demonstrate that HDL reduces vascular A[beta] accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents A[beta]-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering A[beta] binding to collagen-I, ii) forming a complex with A[beta] that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating A[beta] uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE. Conclusion The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to A[beta] and shed new light on a potential role of peripherally-acting apoE in AD. Keywords: Alzheimer's disease, Cerebrovasculature, High-density lipoprotein (HDL), Cerebral amyloid angiopathy (CAA), Endothelial inflammation, Apolipoprotein (apo)E, Tissue engineering Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood. Methods Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces Aβ deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding. Results We demonstrate that HDL reduces vascular Aβ accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents Aβ-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering Aβ binding to collagen-I, ii) forming a complex with Aβ that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating Aβ uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE. Conclusion The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to Aβ and shed new light on a potential role of peripherally-acting apoE in AD. Abstract Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood. Methods Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces Aβ deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding. Results We demonstrate that HDL reduces vascular Aβ accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents Aβ-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering Aβ binding to collagen-I, ii) forming a complex with Aβ that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating Aβ uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE. Conclusion The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to Aβ and shed new light on a potential role of peripherally-acting apoE in AD. Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood. Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces Aβ deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding. We demonstrate that HDL reduces vascular Aβ accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents Aβ-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering Aβ binding to collagen-I, ii) forming a complex with Aβ that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating Aβ uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE. The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to Aβ and shed new light on a potential role of peripherally-acting apoE in AD. Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood. Methods Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces Aβ deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding. Results We demonstrate that HDL reduces vascular Aβ accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents Aβ-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering Aβ binding to collagen-I, ii) forming a complex with Aβ that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating Aβ uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE. Conclusion The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to Aβ and shed new light on a potential role of peripherally-acting apoE in AD. Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid (A[beta]) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood. Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces A[beta] deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding. We demonstrate that HDL reduces vascular A[beta] accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents A[beta]-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering A[beta] binding to collagen-I, ii) forming a complex with A[beta] that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating A[beta] uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE. The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to A[beta] and shed new light on a potential role of peripherally-acting apoE in AD. Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood.BACKGROUNDSeveral lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition and inflammation, however, the mechanisms by which HDL improve cerebrovascular functions relevant to AD remain poorly understood.Here we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces Aβ deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding.METHODSHere we use a human bioengineered model of cerebral amyloid angiopathy (CAA) to define several mechanisms by which HDL reduces Aβ deposition within the vasculature and attenuates endothelial inflammation as measured by monocyte binding.We demonstrate that HDL reduces vascular Aβ accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents Aβ-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering Aβ binding to collagen-I, ii) forming a complex with Aβ that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating Aβ uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE.RESULTSWe demonstrate that HDL reduces vascular Aβ accumulation independently of its principal binding protein, scavenger receptor (SR)-BI, in contrast to the SR-BI-dependent mechanism by which HDL prevents Aβ-induced vascular inflammation. We describe multiple novel mechanisms by which HDL acts to reduce CAA, namely: i) altering Aβ binding to collagen-I, ii) forming a complex with Aβ that maintains its solubility, iii) lowering collagen-I protein levels produced by smooth-muscle cells (SMC), and iv) attenuating Aβ uptake into SMC that associates with reduced low density lipoprotein related protein 1 (LRP1) levels. Furthermore, we show that HDL particles enriched in apolipoprotein (apo)E appear to be the major drivers of these effects, providing new insights into the peripheral role of apoE in AD, in particular, the fraction of HDL that contains apoE.The findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to Aβ and shed new light on a potential role of peripherally-acting apoE in AD.CONCLUSIONThe findings in this study identify new mechanisms by which circulating HDL, particularly HDL particles enriched in apoE, may provide vascular resilience to Aβ and shed new light on a potential role of peripherally-acting apoE in AD. |
| ArticleNumber | 23 |
| Audience | Academic |
| Author | Cashman, Neil R. Silverman, Judith M. Martin, Emma M. Button, Emily B. Gilmour, Megan Boyce, Guilaine Agbay, Andrew Caffrey, Tara M. Robert, Jerome McAlary, Luke Gidden, Zoe Wellington, Cheryl L. Clark, Amanda |
| Author_xml | – sequence: 1 givenname: Jerome orcidid: 0000-0002-2847-9362 surname: Robert fullname: Robert, Jerome email: jrme.robert@gmail.com organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Present address: Institute of Clinical Chemistry, University Hospital Zurich – sequence: 2 givenname: Emily B. surname: Button fullname: Button, Emily B. organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 3 givenname: Emma M. surname: Martin fullname: Martin, Emma M. organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 4 givenname: Luke surname: McAlary fullname: McAlary, Luke organization: Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Department of Physics and Astronomy, University of British Columbia – sequence: 5 givenname: Zoe surname: Gidden fullname: Gidden, Zoe organization: Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 6 givenname: Megan surname: Gilmour fullname: Gilmour, Megan organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 7 givenname: Guilaine surname: Boyce fullname: Boyce, Guilaine organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 8 givenname: Tara M. surname: Caffrey fullname: Caffrey, Tara M. organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 9 givenname: Andrew surname: Agbay fullname: Agbay, Andrew organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 10 givenname: Amanda surname: Clark fullname: Clark, Amanda organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia – sequence: 11 givenname: Judith M. surname: Silverman fullname: Silverman, Judith M. organization: Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Department of Neurology, University of British Columbia – sequence: 12 givenname: Neil R. surname: Cashman fullname: Cashman, Neil R. organization: Department of Neurology, University of British Columbia – sequence: 13 givenname: Cheryl L. surname: Wellington fullname: Wellington, Cheryl L. organization: Department of Pathology and Laboratory Medicine, University of British Columbia, Djavad Mowafaghian Centre for Brain Health, University of British Columbia, School of Biomedical Engineering, University of British Columbia, International Collaboration on Repair Discoveries, University of British Columbia |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32213187$$D View this record in MEDLINE/PubMed |
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| Keywords | Cerebral amyloid angiopathy (CAA) High-density lipoprotein (HDL) Alzheimer’s disease Tissue engineering Apolipoprotein (apo)E Cerebrovasculature Endothelial inflammation |
| Language | English |
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Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular beta-amyloid (Aβ)... Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid (Aβ) deposition... Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid... Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer's disease (AD) risk by decreasing vascular beta-amyloid (A[beta])... Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular beta-amyloid (Aβ)... Abstract Background Several lines of evidence suggest that high-density lipoprotein (HDL) reduces Alzheimer’s disease (AD) risk by decreasing vascular... |
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| SubjectTerms | Advertising executives Alzheimer's disease Apolipoprotein (apo)E Apolipoprotein E Apolipoproteins Apolipoproteins E - metabolism Biomedical and Life Sciences Biomedicine Brain research Cells, Cultured Cerebral amyloid angiopathy Cerebral amyloid angiopathy (CAA) Cerebral Amyloid Angiopathy - metabolism Cerebrovasculature Cholesterol Cholesterol, HDL - metabolism Collagen Disease Diseases EDTA Endothelial inflammation Endothelium Growth factors High density lipoprotein High-density lipoprotein (HDL) Humans Immunotherapy Inflammation Low density lipoprotein receptors Molecular Medicine Monocytes Neurodegenerative diseases Neurology Neurosciences Novels Organ Culture Techniques Pathogenesis Protein binding Proteins Research Article Scavenger receptors Smooth muscle Tissue Engineering Veins & arteries β-Amyloid |
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| Title | Cerebrovascular amyloid Angiopathy in bioengineered vessels is reduced by high-density lipoprotein particles enriched in Apolipoprotein E |
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