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Updated: Mar 31, 2026
Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
CD73 regulates vascular smooth muscle cell functions and facilitates atherosclerotic plaque formation
Jiayin Yang1,2, Rongrong Jian1,3, Jiangang Yu1
1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Abstract:
Extracellular adenosine, generated by ecto-5'-nucleotidase (CD73) via enzymatic catalyzation, has been found to facilitate atherosclerosis (AS). Thus, suppressing CD73 may attenuate AS. In this study, we evaluated the role of CD73 during AS development and further explored cellular and molecular mechanism in smooth muscle cells (SMCs). In a mouse model of carotid artery ligation, inactivation of CD73 inhibited migration and proliferation of vascular SMCs. In in vitro experiments, RNA interference of CD73 inhibited migration, proliferation, and foam cell transformation of human umbilical artery smooth muscle cells. Further, we established an atherosclerotic model using ApoE-/- mice fed with a western diet for 16 weeks. Inactivation of CD73-attenuated AS and hyperlipidemia in ApoE-/- mice. In conclusion, our data suggest that CD73 facilitates AS by promoting migration, proliferation, and foam cell transformation of vascular SMCs and elevating serum lipid levels. Thus, inhibition of CD73 may be beneficial for prevention and treatment of AS.
Insights
Inhibiting ecto-5'-nucleotidase (CD73) reduces atherosclerosis by preventing smooth muscle cell migration, proliferation, and foam cell formation. This suggests CD73 is a potential therapeutic target for treating cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Enzymology
- Molecular Medicine
Background:
- Extracellular adenosine, produced by ecto-5'-nucleotidase (CD73), plays a role in atherosclerosis (AS).
- Targeting CD73 may offer a therapeutic strategy to mitigate AS progression.
Purpose of the Study:
- To investigate the role of CD73 in AS development.
- To elucidate the cellular and molecular mechanisms of CD73 in vascular smooth muscle cells (SMCs).
Main Methods:
- Carotid artery ligation mouse model to assess CD73's effect on SMCs.
- In vitro studies using RNA interference in human umbilical artery SMCs.
- ApoE-/- mice fed a western diet to model AS and hyperlipidemia.
Main Results:
- CD73 inactivation inhibited vascular SMC migration and proliferation in vivo.
- Silencing CD73 reduced migration, proliferation, and foam cell transformation of human SMCs in vitro.
- CD73 deficiency attenuated AS and hyperlipidemia in ApoE-/- mice.
Conclusions:
- CD73 promotes AS by enhancing SMC migration, proliferation, and foam cell transformation.
- CD73 also contributes to hyperlipidemia.
- Inhibiting CD73 presents a potential therapeutic avenue for AS prevention and treatment.
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