ArticleThe Journal of pharmacology and experimental therapeutics2016
Creation of Apolipoprotein C-II (ApoC-II) Mutant Mice and Correction of Their Hypertriglyceridemia with an ApoC-II Mimetic Peptide.
Article in The Journal of pharmacology and experimental therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Establishment and functional analysis of an inducible Apoc2-knockout mouse model to investigate the role of Apoc2 in normal hematopoiesis.Lab animal · 2026Article
- Development of Antisense Oligonucleotide Gapmers for the Treatment of Dyslipidemia and Lipodystrophy.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Lipoprotein lipase requires a flexible lid and stable C-terminal, both maintained by ApoC-II peptide binding.bioRxiv : the preprint server for biology · 2025Article
- Remnant cholesterol predicts the development of type 2 diabetes in patients with nonalcoholic fatty liver disease.Diabetology & metabolic syndrome · 2025Article
- Apolipoprotein CII: Cornerstone of Pathophysiological Interplay in Aortic Stenosis and type 2 Diabetes Mellitus.Aging and disease · 2025Article
- Review
- Short hydrocarbon stapled ApoC2-mimetic peptides activate lipoprotein lipase and lower plasma triglycerides in mice.Frontiers in cardiovascular medicine · 2023Article
- Genetically Engineered Hamster Models of Dyslipidemia and Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Targeting ApoC3 Paradoxically Aggravates Atherosclerosis in Hamsters With Severe Refractory Hypercholesterolemia.Frontiers in cardiovascular medicine · 2022Article
- Triglyceride and Triglyceride-Rich Lipoproteins in Atherosclerosis.Frontiers in molecular biosciences · 2022Review
- HDL Mimetic Peptides.Advances in experimental medicine and biology · 2022Article
- Genetically-engineered hamster models: applications and perspective in dyslipidemia and atherosclerosis-related cardiovascular disease.Medical review (2021) · 2021Article
- Apolipoprotein and LRP1-Based Peptides as New Therapeutic Tools in Atherosclerosis.Journal of clinical medicine · 2021Review
- Review
- Endothelial Cell Receptors in Tissue Lipid Uptake and Metabolism.Circulation research · 2021Review
- Does Proteomic Mirror Reflect Clinical Characteristics of Obesity?Journal of personalized medicine · 2021Article
- Hypertriglyceridemia: new approaches in management and treatment.Current opinion in lipidology · 2020Review
- AAV-Mediated ApoC2 Gene Therapy: Reversal of Severe Hypertriglyceridemia and Rescue of Neonatal Death in ApoC2-Deficient Hamsters.Molecular therapy. Methods & clinical development · 2020Article
- A dual apolipoprotein C-II mimetic-apolipoprotein C-III antagonist peptide lowers plasma triglycerides.Science translational medicine · 2020Article
- Clinical review on triglycerides.European heart journal · 2020Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Apolipoprotein C-II (apoC-II) is a cofactor for lipoprotein lipase, a plasma enzyme that hydrolyzes triglycerides (TGs). ApoC-II deficiency in humans results in hypertriglyceridemia. We used zinc finger nucleases to create Apoc2 mutant mice to investigate the use of C-II-a, a short apoC-II mimetic peptide, as a therapy for apoC-II deficiency. Mutant mice produced a form of apoC-II with an uncleaved signal peptide that preferentially binds high-density lipoproteins (HDLs) due to a 3-amino acid deletion at the signal peptide cleavage site. Homozygous Apoc2 mutant mice had increased plasma TG (757.5 ± 281.2 mg/dl) and low HDL cholesterol (31.4 ± 14.7 mg/dl) compared with wild-type mice (TG, 55.9 ± 13.3 mg/dl; HDL cholesterol, 55.9 ± 14.3 mg/dl). TGs were found in light (density < 1.063 g/ml) lipoproteins in the size range of very-low-density lipoprotein and chylomicron remnants (40-200 nm). Intravenous injection of C-II-a (0.2, 1, and 5 μmol/kg) reduced plasma TG in a dose-dependent manner, with a maximum decrease of 90% occurring 30 minutes after the high dose. Plasma TG did not return to baseline until 48 hours later. Similar results were found with subcutaneous or intramuscular injections. Plasma half-life of C-II-a is 1.33 ± 0.72 hours, indicating that C-II-a only acutely activates lipolysis, and the sustained TG reduction is due to the relatively slow rate of new TG-rich lipoprotein synthesis. In summary, we describe a novel mouse model of apoC-II deficiency and show that an apoC-II mimetic peptide can reverse the hypertriglyceridemia in these mice, and thus could be a potential new therapy for apoC-II deficiency.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.