Hyperoxia impairs pro-angiogenic RNA production in preterm endothelial colony-forming cells
Author
Ahern, Megan A.Black, Claudine P.
Seedorf, Gregory J.
Baker, Christopher D.
Shepherd, Douglas P.
Affiliation
Univ Arizona, Dept PhysiolIssue Date
2017Keywords
single-moleculesingle-cell
fluorescence microscopy
endothelial colony-forming cells
endothelial cell biology
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AMER INST MATHEMATICAL SCIENCES-AIMSCitation
Megan A. Ahern, Claudine P. Black, Gregory J. Seedorf, Christopher D. Baker, Douglas P. Shepherd. Hyperoxia impairs pro-angiogenic RNA production in preterm endothelial colony-forming cells[J]. AIMS Biophysics, 2017, 4(2): 284-297.Journal
AIMS BiophysicsRights
© 2017 Douglas P. Shepherd, et al., licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Disruptions in the response of endothelial progenitor cells to changes in oxygen environment may present a possible mechanism behind multiple pediatric pulmonary disease models, such as bronchopulmonary dysplasia. Using high-throughput fixed single-cell protein and RNA imaging, we have created "stop-motion" movies of Thymosin. 4 (T beta 4) and Hypoxia Inducible Factor 1 alpha (HIF-1 alpha) protein expression and vascular endothelial growth factor (vegf) and endothelial nitric oxide synthase (eNOS) mRNA in human umbilical cord-derived endothelial colony-forming cells (ECFC). ECFC were grown in vitro under both room air and hyperoxia (50% O-2). We find elevated basal T beta 4 protein expression in ECFC derived from prematurely born infants versus full term infants. T beta 4 is a potent growth hormone that additionally acts as an actin sequestration protein and regulates the stability of HIF-1 alpha. This basal level increase of T beta 4 is associated with lower HIF1 alpha nuclear localization in preterm versus term ECFC upon exposure to hyperoxia. We find altered expression in the pro-angiogenic genes vegf and eNOS, two genes that HIF-1 alpha acts as a transcription factor for. This provides a potential link between a developmentally regulated protein and previously observed impaired function of preterm ECFC in response to hyperoxia.Note
Open Access JournalISSN
2377-9098Version
Final published versionSponsors
University of Colorado Denver College of Liberal Arts and Sciences; National Institute of Health [NHLBI HL68702]; National Institutes of Health [K23 HL121090-01A1]Additional Links
http://www.aimspress.com/article/10.3934/biophy.2017.2.284ae974a485f413a2113503eed53cd6c53
10.3934/biophy.2017.2.284
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Except where otherwise noted, this item's license is described as © 2017 Douglas P. Shepherd, et al., licensee AIMS Press. This is an open access article distributed under the terms of the Creative Commons Attribution License.