title: Different oxygen treatment pressures alter inflammatory gene expression in human endothelial cells.
abstract: Hyperbaric oxygen has proven to be a useful treatment for chronic wounds. However, therapeutic conditions vary between treatment centers, and we wished to investigate the effects of different treatment pressures on cells under inflammatory conditions. Endothelial cells were exposed to a chronic wound model comprising hypoxia (2% O2 at 1 atmosphere absolute (atm abs); PO2 approximately 2 kPa) in the presence of 0.5 microg/ml lipopolysaccharide and 1 ng/ml TNF-alpha for 24 hours, then treated with normobaric oxygen (NBO2; 95%O2/5%CO2 at 1.0 atm abs; PO2 approximately 96.3 kPa), hyperbaric oxygen (HBO2) at 1.5 atm abs (1.5HBO2; 96.7%O2/3.3%CO2 at 1.5 atm abs; PO2 approximately 147 kPa), and HBO2 at 2.4 atm abs (2.4HBO2; 97.9%O2/2.1%CO2 at 2.4 atm abs; PO2 approximately 238 kPa). The mRNA expression of 92 inflammatory genes was then analyzed, and we identified changes in genes involved in adhesion molecule expression, angiogenesis and tissue remodeling, intracellular signaling, and cellular oxygen responses and redox signaling. We noted differences in expression between different treatment pressures, highlighting the need for further research into the use of different therapeutic protocols in the treatment of inflammatory conditions such as chronic wounds.
authors.affiliation: University of Exeter Medical School, University of Exeter, Devon, UK.
authors.forename: Alexandra C
authors.initials: AC
authors.lastname: Kendall
authors.forename: Jacqueline L
authors.initials: JL
authors.lastname: Whatmore
authors.forename: Lorna W
authors.initials: LW
authors.lastname: Harries
authors.forename: Paul G
authors.initials: PG
authors.lastname: Winyard
authors.forename: Paul
authors.initials: P
authors.lastname: Eggleton
authors.forename: Gary R
authors.initials: GR
authors.lastname: Smerdon
mesh_terms: D017209:Apoptosis / Q000235:genetics; D001274:Atmospheric Pressure; D015687:Cell Hypoxia / Q000502:physiology; D002908:Chronic Disease; D017719:Diabetic Foot / Q000235:genetics / Q000628:therapy; D005353:Fibronectins / Q000378:metabolism; D015870:Gene Expression / Q000502:physiology; D020869:Gene Expression Profiling / Q000379:methods*; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism*; D006801:Humans; D006931:Hyperbaric Oxygenation / Q000592:standards*; D018836:Inflammation Mediators / Q000378:metabolism*; D018919:Neovascularization, Physiologic / Q000502:physiology; D010084:Oxidation-Reduction; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism*; D014947:Wounds and Injuries / Q000235:genetics / Q000378:metabolism / Q000628:therapy*
chemical_list: C067625:FN1 protein, human; D005353:Fibronectins; D018836:Inflammation Mediators; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D012333:RNA, Messenger