{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Jiang X"],"funding":["NHLBI NIH HHS","NIGMS NIH HHS"],"pagination":["2336-49"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3104770"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(6)"],"pubmed_abstract":["Chronic rejection, manifested as small airway fibrosis (obliterative bronchiolitis [OB]), is the main obstacle to long-term survival in lung transplantation. Recent studies demonstrate that the airways involved in a lung transplant are relatively hypoxic at baseline and that OB pathogenesis may be linked to ischemia induced by a transient loss of airway microvasculature. Here, we show that HIF-1α mediates airway microvascular repair in a model of orthotopic tracheal transplantation. Grafts with a conditional knockout of Hif1a demonstrated diminished recruitment of recipient-derived Tie2⁺ angiogenic cells to the allograft, impaired repair of damaged microvasculature, accelerated loss of microvascular perfusion, and hastened denudation of epithelial cells. In contrast, graft HIF-1α overexpre"],"journal":["The Journal of clinical investigation"],"pubmed_title":["Adenovirus-mediated HIF-1α gene transfer promotes repair of mouse airway allograft microvasculature and attenuates chronic rejection."],"pmcid":["PMC3104770"],"funding_grant_id":["R01 HL082662","P01 HL108797","HL055338","R56 HL082662","R01 HL055338","P20 GM078494","GM078494","HL095686","R01 HL095686","HL082662"],"pubmed_authors":["Tian W","Nicolls MR","Jiang X","Semenza GL","Beilke J","Natarajan R","Khan MA","Kosek J","Yoder MC"],"additional_accession":[]},"is_claimable":false,"name":"Adenovirus-mediated HIF-1α gene transfer promotes repair of mouse airway allograft microvasculature and attenuates chronic rejection.","description":"Chronic rejection, manifested as small airway fibrosis (obliterative bronchiolitis [OB]), is the main obstacle to long-term survival in lung transplantation. Recent studies demonstrate that the airways involved in a lung transplant are relatively hypoxic at baseline and that OB pathogenesis may be linked to ischemia induced by a transient loss of airway microvasculature. Here, we show that HIF-1α mediates airway microvascular repair in a model of orthotopic tracheal transplantation. Grafts with a conditional knockout of Hif1a demonstrated diminished recruitment of recipient-derived Tie2⁺ angiogenic cells to the allograft, impaired repair of damaged microvasculature, accelerated loss of microvascular perfusion, and hastened denudation of epithelial cells. In contrast, graft HIF-1α overexpre","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Jun","modification":"2025-04-25T21:45:37.317Z","creation":"2019-03-27T00:42:08Z"},"accession":"S-EPMC3104770","cross_references":{"pubmed":["21606594"],"doi":["10.1172/JCI46192","10.1172/jci46192"]}}