Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 532, Issue 2, Pages 239-243Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.08.013
Keywords
Transforming growth factor; Smad; Atherosclerosis; Biglycan; TGFBR1; Serine/threonine kinases receptor
Categories
Funding
- National Health and Medical Research Council of Australia [1022800]
- National Heart Foundation of Australia [G09M4385]
- Diabetes Australia Research Trust
- University of Queensland
- National Heart Foundation [102129]
- NHMRC [1160925]
- National Health and Medical Research Council of Australia [1160925] Funding Source: NHMRC
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Pleotropic growth factor, transforming growth factor (TGF)-beta drives the modification and elongation of glycosaminoglycan (GAG) chains on proteoglycans. Hyperelongated GAG chains bind and trap lipoproteins in the intima leading to the formation of atherosclerotic plaques. We have identified that phosphorylation of Smad2 linker region drives GAG chain modification. The identification of an inhibitor of Smad2 linker region phosphorylation and GAG chain modification signifies a potential therapeutic for cardiovascular diseases. Artemisinin renowned for its potent anti-malarial effects possesses a broad range of biological effects. Our aim was to characterise the anti-atherogenic role of artemisinin in vascular smooth muscle cells (VSMCs). We demonstrate that TGF-beta mediated Smad2 linker region phosphorylation and GAG chain elongation was attenuated by artemisinin; however, we observed no effect on VSMC proliferation. Our data demonstrates the potential for artemisinin to be developed as a therapy to inhibit the development of atherosclerosis by prevention of lipid deposition in the vessel wall without affecting the proliferation of VSMCs. (C) 2020 Elsevier Inc. All rights reserved.
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