Journal
LIPIDS IN HEALTH AND DISEASE
Volume 20, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s12944-021-01605-7
Keywords
Apolipoprotein; Triglycerides; Atherosclerosis; CRISPR; Cas9; Rabbit
Funding
- National Key Research and Development Program of China, China [2016YFE0126000]
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APOC3 deficiency in rabbits delays the formation of atherosclerosis induced by a high-fat diet, making it a potential novel therapeutic target for treating atherosclerosis.
Background High levels of apolipoprotein C3 (APOC3) can lead to hypertriglyceridemia, which increases the risk of cardiovascular disease. We aim to create APOC3-knockout (KO) rabbits and explore the effects of APOC3 deletion on the occurrence and development of atherosclerosis. Methods An sgRNA anchored to exon 2 of APOC3 was designed to edit embryo genomes using the CRISPR/Cas9 system. The founder rabbits were sequenced, and their lipid profile, inflammatory cytokines, and atherosclerotic plaques were analyzed. Results When given a normal chow (NC) diet, all APOC3-KO rabbits had 50% lower triglyceride (TG) levels than those of the matched age control group. Additionally, their plasma lipoprotein lipase increased. When fed a high-fat diet, APOC3 deficiency was observed to be more conducive to the maintenance of plasma TG, total cholesterol, and low-density lipoprotein cholesterol levels, and the inhibition of the inflammatory response and the protection against atherosclerosis in rabbits. Conclusion APOC3 deficiency can delay the formation of atherosclerosis-induced HFD in rabbits, indicating this is a novel therapeutic target to treat atherosclerosis.
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