Macrophage MED1 deficiency promotes the development of atherosclerosis in female ApoE and LDLR knockout mice
- VernacularTitle:巨噬细胞MED1缺失促进雌性ApoE和LDLR敲除小鼠动脉粥样硬化发展
- Author:
Ergang WEN
1
,
2
;
Jie GAO
1
,
2
;
Yiming DING
1
,
2
;
Miaoye BAO
1
,
2
;
Yuankun ZHANG
1
,
2
;
Yali ZHANG
1
,
2
;
Sihai ZHAO
1
,
2
;
Enqi LIU
1
,
2
;
Liang BAI
1
,
2
Author Information
- Publication Type:Journal Article
- Keywords: macrophage; MED1; atherosclerosis; gene knockout; female mice
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2023;44(1):89-94
- CountryChina
- Language:Chinese
- Abstract: 【Objective】 To study the effect of macrophage mediator 1 (MED1) deficiency on atherosclerosis in female mice. 【Methods】 ApoE knockout (ApoE-/-), LDLR knockout (LDLR-/-), MED1fl/fl, and macrophage MED1 knockout (MED1△Mac) mice were recruited in the study. Two types of mouse model were constructed:ApoE and macrophage MED1 double knockout (MED1△Mac/ApoE-/-) mice and their littermate controls (MED1fl/fl/ApoE-/-). ② LDLR knockout (LDLR-/-) mice receiving bone marrow from MED1△Mac (MED1△Mac→LDLR-/-) or MED1fl/fl (MED1fl/fl→LDLR-/-) mice. Female mice from these two models were fed a Western diet (21% fat and 0.15% cholesterol) for 12 weeks to promote the development of atherosclerosis. Body weight, total cholesterol (TC), and total triglyceride (TG) content in plasma were measured dynamically. After Western diet feeding for 12 weeks, aortic tree and aortic root were collected and hematoxylin-eosin (H&E) and oil red O staining were performed. 【Results】 Plasma TC and TG did not significantly differ between MED1fl/fl/ApoE-/- control group and MED1△Mac/ApoE-/-experimental group. However, the plaque area in aortic tree and aortic root was significantly increased in MED1△Mac/ApoE-/-mice. Moreover, compared with that in MED1fl/fl→LDLR-/- control group, the plaque area of aortic tree and aortic root had an increasing trend in MED1△Mac→LDLR-/- mice group. 【Conclusion】 MED1 deficiency in macrophages promotes the development of atherosclerosis in female ApoE or LDLR knockout mice.