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Int. J. Mol. Sci. 2016, 17(9), 1484; doi:10.3390/ijms17091484

Effect of Thyrotropin on Osteopontin, Integrin αvβ3, and VCAM-1 in the Endothelium via Activation of Akt

Department of Endocrinology and Metabolism, Institute of Endocrinology, Liaoning Provincial Key Laboratory of Endocrine Diseases, The First Affiliated Hospital of China Medical University, China Medical University, No. 155 Nanjing North Street, Shenyang 110001, Liaoning, China
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Author to whom correspondence should be addressed.
Academic Editor: Masatoshi Maki
Received: 26 July 2016 / Revised: 23 August 2016 / Accepted: 31 August 2016 / Published: 20 September 2016
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

Numerous epidemiological studies have shown that subclinical hypothyroidism (SCH) can impair endothelial function and cause dyslipidemia. Studies have evaluated the effects of thyroid stimulating hormone (TSH) on endothelial cells, but the mechanism underlying the proatherosclerotic effect of increased TSH levels remains unclear. In the present study, SCH rat models were established in thyroidectomized Wistar rats that were given ʟ-T4 daily. The results showed that in vivo, the expression of osteopontin (OPN) vascular cell adhesion molecule (VCAM-1), and levels of integrin αvβ3 in the aortic tissue in SCH and Hypothyroidism (CH) groups was higher than in the control group. However, the effect in the SCH group was higher than in the CH group. In vitro, results showed that different concentration and time gradients of TSH stimulation could increase the expression of OPN, VCAM-1, and integrin αvβ3, and this was accompanied by extracellular signal regulated kinase 1/2 (Erk1/2) and Akt activation in human umbilical vein endothelial cells (HUVECs). TSH induced elevation of these proatherosclerotic factors was partially suppressed by a specific Akt inhibitor but not by a specific Erk inhibitor. Findings suggested that the endothelial dysfunction caused by SCH was related to increased proatherosclerotic factors induced by TSH via Akt activation. View Full-Text
Keywords: thyrotropin; atherosclerosis; subclinical hypothyroidism; osteopontin thyrotropin; atherosclerosis; subclinical hypothyroidism; osteopontin
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MDPI and ACS Style

Yan, Y.; Jiang, F.; Lai, Y.; Wang, H.; Liu, A.; Wang, C.; Zhang, Y.; Teng, W.; Shan, Z. Effect of Thyrotropin on Osteopontin, Integrin αvβ3, and VCAM-1 in the Endothelium via Activation of Akt. Int. J. Mol. Sci. 2016, 17, 1484.

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