التفاصيل البيبلوغرافية
| العنوان: |
CRISPR/Cas9-mediated knockout of APOC3 stabilizes plasma lipids and inhibits atherosclerosis in rabbits |
| المؤلفون: |
Yiwen Zha, Yaoyao Lu, Ting Zhang, Kunning Yan, Wenwen Zhuang, Jingyan Liang, Yong Cheng, Yingge Wang |
| المصدر: |
Lipids in Health and Disease, Vol 20, Iss 1, Pp 1-11 (2021) |
| بيانات النشر: |
BMC, 2021. |
| سنة النشر: |
2021 |
| المجموعة: |
LCC:Nutritional diseases. Deficiency diseases |
| مصطلحات موضوعية: |
Apolipoprotein, Triglycerides, Atherosclerosis, CRISPR/Cas9, Rabbit, Nutritional diseases. Deficiency diseases, RC620-627 |
| الوصف: |
Abstract 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. |
| نوع الوثيقة: |
article |
| وصف الملف: |
electronic resource |
| اللغة: |
English |
| تدمد: |
1476-511X |
| Relation: |
https://doaj.org/toc/1476-511X |
| DOI: |
10.1186/s12944-021-01605-7 |
| URL الوصول: |
https://doaj.org/article/6d69255ef6d9413a90c0714b70226b87 |
| رقم الانضمام: |
edsdoj.6d69255ef6d9413a90c0714b70226b87 |
| قاعدة البيانات: |
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