Name: B6J-Apoe KO Mouse
Brand: 싸이아젠(Cyagen)
SKU: C001507

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B6J-Apoe KO Mouse

제품명

B6J-Apoe KO Mouse

제품 ID

C001507

품종 계통

C57BL/6JCya-Apoe^em1/Cya

Backgroud

C57BL/6JCya

상태

이 마우스 계통을 논문에서 사용할 경우, “B6J-Apoe KO Mouse (카탈로그 번호 C001507)은 Cyagen에서 구입하였습니다.”라고 명시해 주시기 바랍니다.

Disease Animal Models

Atherosclerosis

구매 가능한 제품 종류

연령

Genotype

성별

수량

가격 문의

Disease Animal Models

Atherosclerosis

기본 정보

검증 데이터

The B6J-Apoe KO mouse is a model of ApoE deficiency. It was generated by gene editing technology to knock out the Apoe gene in mice. ApoE protein synthesis is blocked in these mice, leading to elevated cholesterol levels and spontaneous atherosclerosis. Cholesterol levels and atherosclerosis in mice fed a high-fat diet (HFD) are further exacerbated. The B6J-Apoe KO mice are viable and can be used for research in hypercholesterolemia, atherosclerosis, and Alzheimer's disease.

Reference

Huang Y, Mahley RW. Apolipoprotein E: structure and function in lipid metabolism, neurobiology, and Alzheimer's diseases. Neurobiol Dis. 2014 Dec;72 Pt A:3-12.

Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS. J Lipid Res. 2009 Apr;50 Suppl(Suppl): S183-8.

Wang H, Kulas JA, Wang C, Holtzman DM, Ferris HA, Hansen SB. Regulation of beta-amyloid production in neurons by astrocyte-derived cholesterol. Proc Natl Acad Sci U S A. 2021 Aug 17;118(33):e2102191118.

Serrano-Pozo A, Das S, Hyman BT. APOE and Alzheimer's disease: advances in genetics, pathophysiology, and therapeutic approaches. Lancet Neurol. 2021 Jan;20(1):68-80.

Yin C, Ackermann S, Ma Z, Mohanta SK, Zhang C, Li Y, Nietzsche S, Westermann M, Peng L, Hu D, Bontha SV, Srikakulapu P, Beer M, Megens RTA, Steffens S, Hildner M, Halder LD, Eckstein HH, Pelisek J, Herms J, Roeber S, Arzberger T, Borodovsky A, Habenicht L, Binder CJ, Weber C, Zipfel PF, Skerka C, Habenicht AJR. ApoE attenuates unresolvable inflammation by complex formation with activated C1q. Nat Med. 2019 Mar;25(3):496-506.

변형 전략

Figure 1. Gene editing strategy for B6J-Apoe KO mice. Use gene editing technology to knock out the exons 2-4 of the Apoe gene in C57BL/6JCya mice.

응용 분야

Cardiovascular disease research</b>: Hypercholesterolemia, hyperlipidemia, atherosclerosis, etc.;

Body metabolism mechanism research</b>: Fat and cholesterol metabolism;

Neurodegenerative disease research</b>: Alzheimer's disease.

검증 데이터

1. Expression of the APOE protein

Western blot results showed no expression of APOE protein in the livers of B6J-Apoe KO mice.

Figure 2. Expression of APOE protein in the livers of 8-week-old male B6J-Apoe KO and wild-type (WT) mice.

2. Growth Curves

Results showed that B6J-Apoe KO mice grew similarly in normal and HFD conditions. WT mice fed HFD gained weight, and internal inspection data showed that at 20 weeks, the aortic arch and aortic vessels in WT mice were normal and no atherosclerotic plaque was formed.*

*High-fat diet was purchased from Medicience (catalog number: MD12015). High-fat feeding protocol: Mice started gradually transitioning to the high-fat diet at week 5 and began formal feeding on the high-fat diet at week 6.

Figure 3. Body weight trajectories of B6J-Apoe KO and wild-type (WT) mice on normal diet (ND) and high-fat diet (HFD) conditions.

3. Cholesterol blood test in male mice

Data showed that under normal diet conditions, compared with wild-type mice, male B6J-Apoe KO mice had different degrees of increases in triglyceride (TRIG), cholesterol (CHOL), and low-density lipoprotein (LDL-C) levels in their bodies. High-fat diet further increased the levels of these indicators in male B6J-Apoe KO mice. The levels of high-density lipoprotein (HDL-C) in male B6J-Apoe KO and wild-type (WT) mice were not significantly different.

Figure 4. Serum lipid biochemical indicators of male B6J-Apoe KO and wild-type (WT) mice on normal and high-fat diet (HFD) conditions.

4. Cholesterol blood test in female mice

Under normal diet conditions, compared with wild-type mice, female B6J-Apoe KO mice had significantly elevated levels of cholesterol (CHOL) and low-density lipoprotein (LDL-C). High-fat diet further increased the levels of cholesterol (CHOL) and low-density lipoprotein (LDL-C) in female B6J-Apoe KO mice. The levels of high-density lipoprotein (HDL-C) and triglyceride (TRIG) in female B6J-Apoe KO mice and wild-type (WT) mice were not significantly different.

Figure 5. Serum lipid biochemical indicators of female B6J-Apoe KO and wild-type (WT) mice on normal and high-fat diet (HFD) conditions.

5. Aortic pathology in male B6J-Apoe KO mice

Male B6J-Apoe KO mice can spontaneously form atherosclerotic plaques in the aorta after 10 weeks on a normal diet, with mild symptoms. After induction by high-fat diet feeding, the atherosclerotic plaques in the aorta were exacerbated, and the symptoms became more obvious after week 12, continued to worsen at week 14, and reached the late stage of pathological phenotype at week 16.

Figure 6. Detection of atherosclerotic plaques in the aorta of male B6J-Apoe KO mice on normal diet (ND) and high-fat diet (HFD) conditions.

6. Aortic pathology in female B6J-Apoe KO mice

Female B6J-Apoe KO mice can spontaneously form atherosclerotic plaques in the aorta after 12 weeks on a normal diet, with mild symptoms. After induction by high-fat diet feeding, the atherosclerotic plaques in the aorta were exacerbated, and the symptoms became more obvious after week 14 and continued to worsen at week 16.

Figure 7. Detection of atherosclerotic plaques in the aorta of female B6J-Apoe KO mice on normal diet (ND) and high-fat diet (HFD) conditions.

7. Oil Red O staining of the aorta

The red color indicates positive fat staining. The results show that wild-type mice, after 20 weeks of both chow and high-fat diets, exhibited no significant arterial lesions. However, B6J-Apoe KO mice, following a high-fat diet, showed noticeable fat accumulation near the aortic arch, with a more severe phenotype after 20 weeks. Similarly, B6J-Apoe KO mice, after a chow diet, also exhibited spontaneous atherosclerosis, which worsened after 20 weeks.

Figure 8. Oil Red O staining results for B6J-Apoe KO mice and wild-type mice (WT) under chow diet (CD) and high-fat diet (HFD) conditions.

8. Oil Red O staining of cardiac valves

The results show that wild-type mice, after 20 weeks of both chow and high-fat diets, exhibited no fat accumulation near the cardiac valves. However, B6J-Apoe KO mice, following a high-fat diet, showed noticeable fat accumulation near the cardiac valves, with a more severe phenotype after 20 weeks. Similarly, B6J-Apoe KO mice also exhibited fat accumulation under a chow diet, which worsened after 20 weeks.

Figure 9. Oil Red O staining of cardiac valves for B6J-Apoe KO mice and wild-type mice (WT) under chow diet (CD) and high-fat diet (HFD) conditions.

B6J-Apoe KO Mouse

기본 정보

검증 데이터

관련 자료

유전자명

유전자 별칭

NCBI ID

염색체

MGI ID

더보기

Datasheet

품종 계통 설명

Reference

변형 전략

응용 분야

1. Expression of the APOE protein

2. Growth Curves

3. Cholesterol blood test in male mice

4. Cholesterol blood test in female mice

5. Aortic pathology in male B6J-Apoe KO mice

6. Aortic pathology in female B6J-Apoe KO mice

7. Oil Red O staining of the aorta

8. Oil Red O staining of cardiac valves

관련 제품

리소스

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