Journal article
Shear Stress-Induced NO Production is Dependent on ATP Autocrine Signaling and Capacitative Calcium Entry
Cellular and molecular bioengineering, v 7(4), pp 510-520
01 Dec 2014
PMID: 25386222
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Flow-induced production of nitric oxide (NO) by endothelial cells plays a fundamental role in vascular homeostasis. However, the mechanisms by which shear stress activates NO production remain unclear due in part to limitations in measuring NO, especially under flow conditions. Shear stress elicits the release of ATP, but the relative contribution of autocrine stimulation by ATP to flow-induced NO production has not been established. Furthermore, the importance of calcium in shear stress-induced NO production remains controversial, and in particular the role of capacitive calcium entry (CCE) has yet to be determined. We have utilized our unique NO measurement device to investigate the role of ATP autocrine signaling and CCE in shear stress-induced NO production. We found that endogenously released ATP and downstream activation of purinergic receptors and CCE plays a significant role in shear stress-induced NO production. ATP-induced eNOS phophorylation under static conditions is also dependent on CCE. Inhibition of protein kinase C significantly inhibited eNOS phosphorylation and the calcium response. To our knowledge, we are the first to report on the role of CCE in the mechanism of acute shear stress-induced NO response. In addition, our work highlights the importance of ATP autocrine signaling in shear stress-induced NO production.
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Details
- Title
- Shear Stress-Induced NO Production is Dependent on ATP Autocrine Signaling and Capacitative Calcium Entry
- Creators
- Allison M. Andrews - Drexel UniversityDov Jaron - Drexel UniversityDonald G. Buerk - Drexel UniversityKenneth A. Barbee - Drexel University
- Publication Details
- Cellular and molecular bioengineering, v 7(4), pp 510-520
- Publisher
- Springer Nature
- Number of pages
- 11
- Grant note
- R01HL068164 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems; [Retired Faculty]
- Web of Science ID
- WOS:000344646900003
- Scopus ID
- 2-s2.0-84939897431
- Other Identifier
- 991019168682404721
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InCites Highlights
Data related to this publication, from InCites Benchmarking & Analytics tool:
- Web of Science research areas
- Biophysics
- Cell & Tissue Engineering
- Cell Biology
- Engineering, Biomedical