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Author Notes:

Address correspondence to W. Robert Taylor, Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA. wtaylor@emory.edu

Associate Editor Jin-Yu Shao oversaw the review of this article.

Christa Caesar, Alicia N. Lyle, Giji Joseph, Daiana Weiss, Fadi M. F. Alameddine, Bernard Lassègue, Kathy K. Griendling, and W. Robert Taylor have no conflicts of interest to disclose.

This article does not contain any studies with human participants performed by any of the authors.

All applicable international, national, and/or institutional guidelines for the care and use of animals were followed.


Research Funding:

This work was supported by National Institutes of Health (NIH) PO1 HL095070 (WRT and KKG) and a pre-doctoral Grant from the American Heart Association (CC).


  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell & Tissue Engineering
  • Biophysics
  • Cell Biology
  • Angiotensin II
  • Norepinephrine
  • Cyclic strain
  • Inflammation
  • Vascular hypertrophy
  • Smooth muscle cells

Cyclic Strain and Hypertension Increase Osteopontin Expression in the Aorta


Journal Title:

Cellular and Molecular Bioengineering


Volume 10, Number 2


, Pages 144-152

Type of Work:

Article | Post-print: After Peer Review


Hypertension has a direct impact on vascular hypertrophy and is a known risk factor for the development of atherosclerosis. Osteopontin (OPN) has emerged as an important protein mediator of inflammation and remodeling of large arteries. However, its role and mechanism of regulation in the setting of hypertension is still unknown. Our objectives for this study were therefore to investigate the role of OPN in hypertension-induced vascular remodeling and inflammation. OPN Knockout (KO) and wild type (WT) mice were made hypertensive with angiotensin II (Ang II) infusion for seven days. We observed that OPN KO aortas were protected against Ang II-induced medial hypertrophy and inflammation, despite comparable increases in systolic blood pressure (SBP) in both groups. OPN expression was increased in WT aortas from hypertensive mice (induced by either Ang II or norepinephrine). OPN expression was increased in aortic smooth muscle cells (SMCs) subjected to cyclic mechanical strain suggesting that mechanical deformation of the aortic wall is responsible in part for the increased OPN expression induced by hypertension. Finally, we utilized hypertensive transgenic smooth muscle cell-specific catalase overexpressing (Tg SMC-Cat ) mice to determine the role of H 2 O 2 in mediating hypertension-induced increases in OPN expression. We also found that the hypertension-induced increase in OPN expression was inhibited in transgenic smooth muscle cell-specific catalase overexpressing (Tg SMC-Cat ) mice, suggesting that H 2 O 2 , plays a vital role in mediating the hypertension-induced increase in OPN expression. Taken together, these results define a potentially important role for OPN in the pathophysiology of hypertension.

Copyright information:

© 2016, Biomedical Engineering Society.

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