Overexpression of PER2 inhibits the progression of atherosclerosis via the Akt-eNOS signaling in apolipoprotein e-null mice
Atherosclerosis is an inflammatory disease. The circadian clock gene has a connection with inflammation, including vascular inflammation. However, whether circadian clock gene has a regulatory effect on atherosclerosis is rarely studied. Our aim is to determine whether Period 2 (Per2), a main clock gene, exerts a therapeutical effect on atherosclerosis in Apolipoprotein E-null (ApoE-/-) mice. Atherosclerotic mice were divided into three groups, including the Control group (mice received an intravenous injection of phosphate buffered saline at 13 weeks old), the Ad-GFP group (mice received an intravenous infection of adenovirus vector carrying GFP at 13 weeks old) and the Ad-PER2 group (mice received an intravenous infection of adenovirus vector carrying PER2 at 13 weeks old). PER2 overexpression decreased lesion areas of aorta and aortic root, levels of inflammatory factors and adhesion molecules, and the serum levels of total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C). Moreover, PER2 exerted an inhibitory effect on atherosclerosis by activating the protein kinase B-endothelial nitric oxide synthase (Akt-eNOS) signaling pathway in ApoE-/- mice. Taken together, our findings suggest that PER2 has an inhibitory effect on atherosclerosis in ApoE-/- mice via activation of the Akt-eNOS pathway.
Authors: Gang Su1*, Guangli Sun2*, Hai Liu1 , Liliang Shu1 , Jingchao Zhang1 , Longhui Guo1 , Chen Huang1 , Jing Xu1
Influence Factor: 1.7059
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