Hyperoxia impairs pro-angiogenic RNA production in preterm endothelial colony-forming cells
AuthorAhern, Megan A.
Black, Claudine P.
Seedorf, Gregory J.
Baker, Christopher D.
Shepherd, Douglas P.
AffiliationUniv Arizona, Dept Physiol
endothelial colony-forming cells
endothelial cell biology
MetadataShow full item record
PublisherAMER INST MATHEMATICAL SCIENCES-AIMS
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.
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.
Collection InformationThis 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 firstname.lastname@example.org.
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.
NoteOpen Access Journal
VersionFinal published version
SponsorsUniversity of Colorado Denver College of Liberal Arts and Sciences; National Institute of Health [NHLBI HL68702]; National Institutes of Health [K23 HL121090-01A1]
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.