<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">OWINGS, RICHARD A.</style></author><author><style face="normal" font="default" size="100%">BOERMA, MARJAN</style></author><author><style face="normal" font="default" size="100%">WANG, JUNRU</style></author><author><style face="normal" font="default" size="100%">BERBEE, MAAIKE</style></author><author><style face="normal" font="default" size="100%">LADEROUTE, KEITH R.</style></author><author><style face="normal" font="default" size="100%">SODERBERG, LEE S.F.</style></author><author><style face="normal" font="default" size="100%">VURAL, EMRE</style></author><author><style face="normal" font="default" size="100%">JENSEN, MARTIN HAUER</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Selective Deficiency of HIF-1α in Myeloid Cells Influences Secondary Intention Wound Healing in Mouse Skin</style></title><secondary-title><style face="normal" font="default" size="100%">In Vivo</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2009-11-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">879-884</style></pages><volume><style face="normal" font="default" size="100%">23</style></volume><issue><style face="normal" font="default" size="100%">6</style></issue><abstract><style  face="normal" font="default" size="100%">Background: Hypoxia-inducible factor-1 (HIF-1) influences myeloid cell function. In this study we examined the role of myeloid cell HIF-1α on wound healing in vivo using a cell-specific knockout (KO) mouse model. Materials and Methods: HIF-1α KO mice and wild-type (WT) controls received 8 mm full thickness dorsal dermal wounds. Wound dimensions were measured until full closure. Tissue was obtained from 3-day-old wounds for (immuno-)histochemical analysis. Production of interleukin-1β (IL-1β) and nitric oxide (NO) in response to lipopolysaccharide (LPS) and/or desferrioxamine (DFX) was examined in vitro. Results: Early wound closure occurred significantly faster in HIF-1α KO mice than in WT mice. Wounds of KO mice contained similar numbers of neutrophils and macrophages, but more activated keratinocytes, consistent with accelerated re-epithelialization. Interestingly, while LPS and LPS+DFX elicited a similar IL-1β response in macrophages from the 2 mouse types, NO production was blunted in HIF-1α KO macrophages. Conclusion: Absence of HIF-1α in myeloid cells accelerates the early phase of secondary intention wound healing in vivo. This may be associated with a deficient ability of myeloid cells to initiate an appropriate NO production response. Pharmacologic modulators of HIF-1α should be explored in situations with abnormal wound healing.</style></abstract></record></records></xml>