caa a22 4500 605521069 CHVBK 20210128100738.0 cr unu---uuuuu 210128e20150101xx s 000 0 eng 10.1007/s00223-014-9934-8 doi (NATIONALLICENCE)springer-10.1007/s00223-014-9934-8 Thyroid Hormone Attenuates Vascular Calcification Induced by Vitamin D3 Plus Nicotine in Rats [Elektronische Daten] [Jing Zhang, Jin-Rui Chang, Xiao-Hui Duan, Yan-Rong Yu, Bao-Hong Zhang] Thyroid hormones (THs) including thyroxine (T4) and triiodothyronine (T3) play critical roles in bone remodeling. However, the role and mechanism of THs in vascular calcification (VC) have been unclear. To explore the pathophysiological roles of T3 on VC, we investigated the changes in plasma and aortas of THs concentrations and the effect of T3 on rat VC induced by vitamin D3 plus nicotine (VDN). VDN-treated rat showed decreased plasma T3 content, increased vascular calcium deposition, and alkaline phosphatase (ALP) activity. Administration of T3 (0.2mg/kg body weight IP) for 10days greatly reduced vascular calcium deposition and ALP activity in calcified rat aortas when compared with controls. Concurrently, the loss of smooth muscle lineage markers α-actin and SM22a was restored, and the increased bone-associated molecules, such as runt-related transcription factor2 (Runx2), Osterix, and osteopontin (OPN) levels in calcified aorta, were reduced by administration of T3. The suppression of klotho in calcified rat aorta was restored by T3. Methimazole (400mg/L) blocked the beneficial effect of T3 on VC. These results suggested that T3 can inhibit VC development. Springer Science+Business Media New York, 2014 Thyroid hormone nationallicence Vascular calcification nationallicence Vitamin D3 plus nicotine nationallicence Zhang Jing School of P.E. and Sports Science, Beijing Normal University, 100875, Beijing, China aut Chang Jin-Rui Laboratory of Cardiovascular Bioactive Molecules, School of Basic Medical Sciences, Peking University, 100191, Beijing, China aut Duan Xiao-Hui Laboratory of Cardiovascular Bioactive Molecules, School of Basic Medical Sciences, Peking University, 100191, Beijing, China aut Yu Yan-Rong Laboratory of Cardiovascular Bioactive Molecules, School of Basic Medical Sciences, Peking University, 100191, Beijing, China aut Zhang Bao-Hong Hospital of Tsinghua University, 100084, Beijing, China aut Calcified Tissue International Springer US; http://www.springer-ny.com 96/1(2015-01-01), 80-87 0171-967X 96:1<80 2015 96 223 https://doi.org/10.1007/s00223-014-9934-8 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s00223-014-9934-8 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Zhang Jing School of P.E. and Sports Science, Beijing Normal University, 100875, Beijing, China aut NATIONALLICENCE 700 1- Chang Jin-Rui Laboratory of Cardiovascular Bioactive Molecules, School of Basic Medical Sciences, Peking University, 100191, Beijing, China aut NATIONALLICENCE 700 1- Duan Xiao-Hui Laboratory of Cardiovascular Bioactive Molecules, School of Basic Medical Sciences, Peking University, 100191, Beijing, China aut NATIONALLICENCE 700 1- Yu Yan-Rong Laboratory of Cardiovascular Bioactive Molecules, School of Basic Medical Sciences, Peking University, 100191, Beijing, China aut NATIONALLICENCE 700 1- Zhang Bao-Hong Hospital of Tsinghua University, 100084, Beijing, China aut NATIONALLICENCE 773 0- Calcified Tissue International Springer US; http://www.springer-ny.com 96/1(2015-01-01), 80-87 0171-967X 96:1<80 2015 96 223