| First Author | Liang W | Year | 2018 |
| Journal | Cell Physiol Biochem | Volume | 45 |
| Issue | 4 | Pages | 1434-1443 |
| PubMed ID | 29466783 | Mgi Jnum | J:274093 |
| Mgi Id | MGI:6284915 | Doi | 10.1159/000487569 |
| Citation | Liang W, et al. (2018) Knockout of Low Molecular Weight FGF2 Attenuates Atherosclerosis by Reducing Macrophage Infiltration and Oxidative Stress in Mice. Cell Physiol Biochem 45(4):1434-1443 |
| abstractText | BACKGROUND/AIMS: Fibroblast growth factor 2 (FGF2) plays a predominant role during angiogenesis in the adventitia and in atherosclerotic plaque. A dilemma exists, however, as to whether angiogenic stimulation by FGF2 for the prevention and treatment of atherogenesis is feasible. The aim of this study is to investigate the effect of the 18-kDa FGF-2 isoform on atherosclerosis progression in high-fat diet-fed apolipoprotein E knockout (ApoE-/-) mice. METHODS: We established a model of atherosclerosis using ApoE and 18-kDa FGF-2 gene double knockout mice. They were randomly divided into three groups depending on the duration of diet: 8 weeks, 12 weeks and 16 weeks. Then, we studied the morphology and inflammatory factor staining in the atherosclerosis plaque of these mice. RESULTS: Knockout of the 18-kDa FGF-2 isoform did not change the metabolic characteristics of the mice. Compared to the control group, knockout of the 18-kDa FGF-2 isoform significantly attenuated atherogenesis, reduced aortic plaques, reduced macrophage infiltration and suppressed oxidative stress in mice fed with a high fat diet at all-time points. CONCLUSIONS: 18-kDa FGF-2 aggravated the inflammatory reaction of atherosclerosis. |
