ArticleJournal of liposome research2014
Nanoliposomes protect against AL amyloid light chain protein-induced endothelial injury.
Article in Journal of liposome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- In vitro and in vivo disease models of cardiac amyloidosis: progress, pitfalls, and potential.Cardiovascular research · 2025Review
- Engineered Nanoparticle-Protein Interactions Influence Protein Structural Integrity and Biological Significance.Nanomaterials (Basel, Switzerland) · 2022Review
- Mechanistic Insights into the Early Events in the Aggregation of Immunoglobulin Light Chains.Biochemistry · 2019Article
- PEGylated-nanoliposomal clusterin for amyloidogenic light chain-induced endothelial dysfunction.Journal of liposome research · 2018Article
- Is Vascular Amyloidosis Intertwined with Arterial Aging, Hypertension and Atherosclerosis?Frontiers in genetics · 2017Review
- Monosialoganglioside-Containing Nanoliposomes Restore Endothelial Function Impaired by AL Amyloidosis Light Chain Proteins.Journal of the American Heart Association · 2016Article
- Nanoliposomes protect against human arteriole endothelial dysfunction induced by β-amyloid peptide.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Adipose and leptomeningeal arteriole endothelial dysfunction induced by β-amyloid peptide: a practical human model to study Alzheimer's disease vasculopathy.Journal of neuroscience methods · 2014Article
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Authors and funding
11 authors at 6 institutions in 1 country.
Funding
Abstract
contextA newly-recognized pathogenic mechanism underlying light chain amyloidosis (AL) involves endothelial dysfunction and cell injury caused by misfolded light chain proteins (LC). Nanoliposomes (NL) are artificial phospholipid vesicles that could attach to misfolded proteins and reduce tissue injury.
objectiveTo test whether co-treatment with NL reduces LC-induced endothelial dysfunction and cell death.
methodsAbdominal subcutaneous adipose arterioles from 14 non-AL subjects were cannulated; dilator response to acetylcholine and papaverine were measured at baseline and following 1-hour exposure to LC (20 µg/mL, 2 purified from AL subjects' urine, 1 from human recombinant LC [AL-09]) ± NL (phosphatidylcholine/cholesterol/phosphatidic acid 70/25/5 molar ratio) or NL alone. Human aortic artery endothelial cells (HAEC) were exposed to Oregon Green-labeled LC ± NL for 24 hours and intracellular LC and apoptosis (Hoechst stain) were measured. Circular dichroism spectroscopy was performed on AL-09 LC ± NL to follow changes in secondary structure and protein thermal stability.
resultsLC caused impaired dilation to acetylcholine that was restored by NL (control - 94.0 ± 1.8%, LC - 65.0 ± 7.1%, LC + NL - 95.3 ± 1.8%, p ≤ 0.001 LC versus control or LC + NL). NL protection was inhibited by L-NG-nitroarginine methyl ester. NL increased the beta sheet structure of LC, reduced endothelial cell internalization of LC and protected against LC-induced endothelial cell death.
conclusionsLC induced human adipose arteriole endothelial dysfunction and endothelial cell death, which were reversed by co-treatment with NL. This protection may partly be due to enhancing LC protein structure and reducing LC internalization. Nanoliposomes represent a promising new class of agents to ameliorate tissue injury from protein misfolding diseases such as AL.
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