Abstract
Atherosclerosis (AS) is a leading chronic diseases with high death rate in industrialized countries, where AS is caused by many factors. Studies show that tight junction protein (TJP) and Connexin family play important roles in heart and blood vessel function and health. Changing Gap Junction Protein (Cx43 Cx45 and Cx46) and Tight Junction Protein (Zo-1, Claudin-1 and Occludin-1) may have effects on AS pathogenesis. Here, we construct a rat model on a high-fat diet to explain the relationship between atherosclerosis pathogenesis and TJP/GJP changes. Our results showed that compared with control group, the weight of treatment group increased significantly with the formation of atheromas and the artery wall infiltration with adipose tissue in histological section. Our qPCR and western blotting results of heart coronary and artery endothelial tissue showed that Cx43/45/46 and claudin-1 were significantly down-regulated in coronary artery. In FITC-Inulin transwell experiment, a paracellular permeability test, we found that primary endothelial cell of high-fat diet rat group showed higher permeability compared to control group. Imunofluorescence staining experiment showed less Cx43 and Zo-1 protein expression and more CD14 monocyte penetration in heart and aorta wall in high-fat diet rat group. Our results suggested that atheroma formation might be due to the loss of TJP and GJP, causing higher permeability in rat coronary artery and thus promoted the pathogenesis of atherosclerosis.
| Original language | English |
|---|---|
| Pages (from-to) | 7969-7976 |
| Number of pages | 8 |
| Journal | International Journal of Clinical and Experimental Pathology |
| Volume | 9 |
| Issue number | 8 |
| Publication status | Published - 2016 |
| Externally published | Yes |
Keywords
- Atherosclerosis
- Gap junction protein
- Tight junction protein