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Int. J. Mol. Sci. 2016, 17(3), 266; doi:10.3390/ijms17030266

Endogenous Sulfur Dioxide Inhibits Vascular Calcification in Association with the TGF-β/Smad Signaling Pathway

1
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China
2
Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100191, China
3
Department of Medical and Health Sciences, Linköping University, Linköping 58183, Sweden
4
Department of Physiology and Pathophysiology, Peking University Health Science Centre, Beijing 100191, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Joseph V. Moxon
Received: 31 December 2015 / Revised: 31 January 2016 / Accepted: 5 February 2016 / Published: 23 February 2016
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

The study was designed to investigate whether endogenous sulfur dioxide (SO2) plays a role in vascular calcification (VC) in rats and its possible mechanisms. In vivo medial vascular calcification was induced in rats by vitamin D3 and nicotine for four weeks. In vitro calcification of cultured A7r5 vascular smooth muscle cells (VSMCs) was induced by calcifying media containing 5 mmol/L CaCl2. Aortic smooth muscle (SM) α-actin, runt-related transcription factor 2 (Runx2), transforming growth factor-β (TGF-β) and Smad expression was measured. VC rats showed dispersed calcified nodules among the elastic fibers in calcified aorta with increased aortic calcium content and alkaline phosphatase (ALP) activity. SM α-actin was markedly decreased, but the osteochondrogenic marker Runx2 concomitantly increased and TGF-β/Smad signaling was activated, in association with the downregulated SO2/aspartate aminotransferase (AAT) pathway. However, SO2 supplementation successfully ameliorated vascular calcification, and increased SM α-actin expression, but inhibited Runx2 and TGF-β/Smad expression. In calcified A7r5 VSMCs, the endogenous SO2/AAT pathway was significantly downregulated. SO2 treatment reduced the calcium deposits, calcium content, ALP activity and Runx2 expression and downregulated the TGF-β/Smad pathway in A7r5 cells but increased SM α-actin expression. In brief, SO2 significantly ameliorated vascular calcification in association with downregulation of the TGF-β/Smad pathway. View Full-Text
Keywords: sulfur dioxide; vascular calcification; smooth muscle cell; transforming growth factor-β sulfur dioxide; vascular calcification; smooth muscle cell; transforming growth factor-β
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MDPI and ACS Style

Li, Z.; Huang, Y.; Du, J.; Liu, A.D.; Tang, C.; Qi, Y.; Jin, H. Endogenous Sulfur Dioxide Inhibits Vascular Calcification in Association with the TGF-β/Smad Signaling Pathway. Int. J. Mol. Sci. 2016, 17, 266.

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