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Irisin Inhibits Atherosclerosis by Promoting Endothelial Proliferation Through microRNA126-5p
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نویسنده
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zhang y. ,song h. ,zhang y. ,wu f. ,mu q. ,jiang m. ,wang f. ,zhang w. ,li l. ,shao l. ,li s. ,yang l. ,zhang m. ,wu q. ,tang d.
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منبع
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journal of the american heart association - 2016 - دوره : 5 - شماره : 9
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چکیده
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Background: irisin is a newly discovered myokine that has been considered a promising candidate for the treatment of cardiovascular disease through improving endothelial function. however,little is known about the role of irisin in the progression of atherosclerosis. methods and results: we used a carotid partial ligation model of apolipoprotein e-deficient mice fed on a high-cholesterol diet to test the anti-atherosclerosis effect of irisin. irisin treatment significantly suppressed carotid neointima formation. it was associated with increased endothelial cell proliferation. in addition,irisin promoted human umbilical vein endothelial cell survival via upregulating microrna126-5p expression through the erk signaling pathway. inhibition of microrna126-5p using the microrna126-5p inhibitor abolished the prosurvival effect. the same results were demonstrated in vivo as the expression of microrna126-5p noticeably increased in ligated carotid artery after irisin treatment. furthermore,in vivo blockade of microrna126-5p expression using the antagomir abolished the inhibitory effects of irisin on neointima formation,lesional lipid deposition,macrophage area,and the pro-proliferation effects on endothelial cells. conclusions: taken together,our study demonstrates that irisin significantly reduces atherosclerosis in apolipoprotein e-deficient mice via promoting endothelial cell proliferation through microrna126-5p,which may have a direct therapeutic effect on atherosclerotic diseases. © 2016 the authors. published on behalf of the american heart association,inc.,by wiley blackwell.
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کلیدواژه
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Atherosclerosis; Endothelial cells; Irisin; MicroRNA126-5p
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آدرس
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center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China, department of pathology,immunology,and laboratory medicine,university of florida college of medicine,gainesville,fl, United States, department of pathology,immunology,and laboratory medicine,university of florida college of medicine,gainesville,fl, United States, the key laboratory of cardiovascular remodeling and function research,chinese ministry of education and chinese ministry of health,qilu hospital of shandong university,jinan, China, department of anatomy,school of medicine shandong university,jinan, China, center for gene therapy and immunotherapy,the second hospital of shandong university,jinan, China
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Authors
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