KLF7 in epicardial adipose tissue of coronary heart disease promotes inflammation and adipose differentiation
10.19405/j.cnki.issn1000-1492.2022.02.007
- Author:
Yajun Xue
1
,
2
;
Wenhua Huang
1
;
Yayan Du
1
,
3
;
Yijun Zhou
1
;
Xingxing Dong
1
;
Yutao Wei
1
,
4
Author Information
1. Dept of Medicine , Shihezi University, Xinjiang Key Laboratory of Ethnic and Endemic Diseases , Ministry of Education , Shihezi 832000
2. Dept of Thoracic and Cardiovascular Surgery, The First Afiliated Hospital of Shihezi University School of Medicine , Shihezi 832008
3. Emergency Center of Jingzhou Central Hospital , Jingzhou 434000
4. Dept of Thoracic Surgery, Jining First People Hospital , Jining 272000
- Publication Type:Journal Article
- Keywords:
coronary heart disease;
epicardial adipose tissue;
KLF7;
macrophages;
inflammation
- From:
Acta Universitatis Medicinalis Anhui
2022;57(2):197-202
- CountryChina
- Language:Chinese
-
Abstract:
Objective :To explore the epicardial adipose tissue ( EAT) of patients with coronary heart disease , KLF7 stimulates macrophages to secrete inflammatory factors and promotes the differentiation and maturation of adipocytes through the NF⁃κB signaling pathway , and to clarify the mechanism of KLF7 in the occurrence and development of CAD.
Methods :30 patients with coronary heart disease ( CAD group) and 30 patients without coronary heart disease (non⁃CAD group) were collected , and general data and biochemical indicators were collected. qRT⁃PCR was used to detect the expression levels of KLF7 , APN , IL⁃6 , and TNF⁃α mRNA in EAT. Human THP⁃1 cells were cultured in vitro and induced into M1 type macrophages and 3T3 ⁃L1 preadipocytes. The cells were divied into 3 groups : KLF7 up⁃regulated group ( transfected with KLF7 mimic) , KLF7 down⁃regulated group ( transfected with siRNA knockdown KLF7 ) , NC group ( transfected oligopeptide sequence) , transfected two kinds of cells. qRT⁃PCR was used to detect the expression of APN , MCP⁃1 , IL⁃6 and TNF⁃α mRNA in M1 type macrophages , and the protein expression levels of key factors in the NF⁃κB signaling pathway were detected by Westren blot.
The qRT⁃PCR method was used to detect APN , KLF4 , IL⁃6 , MCP⁃1 mRNA and adipocyte differentiation marker peroxisome proliferator⁃activated receptor⁃γ (PPARγ) in 3T3 ⁃L1 preadipocytes 24 h after transfection. CCAAT/enhancer binding protein α (C/EBPα ) , fatty acid binding protein 4 (FABP4) mRNA relative expression levels , and Westren blot was used to detect protein expression levels.
Results : Compared with the non⁃CAD group , the expression of CAD group decreased , APN decreased , IL⁃6 and TNF⁃α increased significantly , and the difference was statistically significant (P < 0. 01) . KLF7 was highly expressed in human THP⁃1 derived M1 macrophages induced by inflammatory stimuli (LPS) . In M1 macrophages derived from human THP⁃1 , knocking down KLF7 could inhibit the release of inflammatory factors. Transfection with KLF7 ⁃siRNA could significantly inhibit LPS⁃induced phosphorylation of JNK⁃MAPKs , the level of p⁃p65 and the activation of p ⁃IκBa (P < 0. 05) . In 3T3 ⁃L1 preadipocytes , upregulation of KLF7 increased the expression of adipocyte differentiation markers PPARγ , C/EBPa , FABP4 mRNA , and promoted the differentiation of 3T3 ⁃L1 preadipocytes into adipocytes (P < 0. 05) .
Conclusion:The expression of KLF7 in EAT in CAD patients increases. KLF7 activates the activation of macrophages mediated by the JNK⁃NF⁃KB signaling pathway in EAT , promotes inflammation in EAT in CAD patients , and promotes the differentiation and maturation of adipocytes , thereby promoting the development of CAD. It indicates that KLF7 may be a potential therapeutic target for cardiovascular diseases (such as CAD) .
- Full text:2024120511321014786冠心病心外膜脂肪组织中KL...促进炎症反应及脂肪分化成熟_薛亚军 (1).pdf
