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dc.contributor.authorAhern, Megan A.
dc.contributor.authorBlack, Claudine P.
dc.contributor.authorSeedorf, Gregory J.
dc.contributor.authorBaker, Christopher D.
dc.contributor.authorShepherd, Douglas P.
dc.date.accessioned2017-11-17T19:30:40Z
dc.date.available2017-11-17T19:30:40Z
dc.date.issued2017
dc.identifier.citationMegan 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.en
dc.identifier.issn2377-9098
dc.identifier.doi10.3934/biophy.2017.2.284
dc.identifier.urihttp://hdl.handle.net/10150/626103
dc.description.abstractDisruptions 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.
dc.description.sponsorshipUniversity of Colorado Denver College of Liberal Arts and Sciences; National Institute of Health [NHLBI HL68702]; National Institutes of Health [K23 HL121090-01A1]en
dc.language.isoenen
dc.publisherAMER INST MATHEMATICAL SCIENCES-AIMSen
dc.relation.urlhttp://www.aimspress.com/article/10.3934/biophy.2017.2.284en
dc.rights© 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.en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectsingle-moleculeen
dc.subjectsingle-cellen
dc.subjectfluorescence microscopyen
dc.subjectendothelial colony-forming cellsen
dc.subjectendothelial cell biologyen
dc.titleHyperoxia impairs pro-angiogenic RNA production in preterm endothelial colony-forming cellsen
dc.typeArticleen
dc.contributor.departmentUniv Arizona, Dept Physiolen
dc.identifier.journalAIMS Biophysicsen
dc.description.noteOpen Access Journalen
dc.description.collectioninformationThis 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.en
dc.eprint.versionFinal published versionen
refterms.dateFOA2018-09-12T00:10:54Z
html.description.abstractDisruptions 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.


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© 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.
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.