{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T19:41:59Z","timestamp":1790797319313,"version":"4.1.0"},"reference-count":82,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","license":[{"start":{"date-parts":[[2023,8,1]],"date-time":"2023-08-01T00:00:00Z","timestamp":1690848000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>During infectious diseases, proinflammatory cytokines transiently destabilize interactions between adjacent vascular endothelial cells (ECs) to facilitate the passage of immune molecules and cells into tissues. However, in the lung, the resulting vascular hyperpermeability can lead to organ dysfunction. Previous work identified the transcription factor ERG (erythroblast transformation-specific\u2013related gene) as a master regulator of endothelial homeostasis. Here we investigate whether the sensitivity of pulmonary blood vessels to cytokine-induced destabilization is due to organotypic mechanisms affecting the ability of endothelial ERG to protect lung ECs from inflammatory injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      Cytokine-dependent ubiquitination and proteasomal degradation of ERG were analyzed in cultured HUVECs (human umbilical vein ECs). Systemic administration of TNF\u03b1 (tumor necrosis factor alpha) or the bacterial cell wall component lipopolysaccharide was used to cause a widespread inflammatory challenge in mice; ERG protein levels were assessed by immunoprecipitation, immunoblot, and immunofluorescence. Murine\n                      <jats:italic toggle=\"yes\">Erg<\/jats:italic>\n                      deletion was genetically induced in ECs (\n                      <jats:italic toggle=\"yes\">\n                        Erg\n                        <jats:sup>fl\/fl<\/jats:sup>\n                        ;Cdh5[PAC]-Cre\n                        <jats:sup>ERT2<\/jats:sup>\n                      <\/jats:italic>\n                      ), and multiple organs were analyzed by histology, immunostaining, and electron microscopy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      In vitro, TNF\u03b1 promoted the ubiquitination and degradation of ERG in HUVECs, which was blocked by the proteasomal inhibitor MG132. In vivo, systemic administration of TNF\u03b1 or lipopolysaccharide resulted in a rapid and substantial degradation of ERG within lung ECs but not ECs of the retina, heart, liver, or kidney. Pulmonary ERG was also downregulated in a murine model of influenza infection.\n                      <jats:italic toggle=\"yes\">\n                        Erg\n                        <jats:sup>fl\/fl<\/jats:sup>\n                        ;Cdh5(PAC)-Cre\n                        <jats:sup>ERT2<\/jats:sup>\n                      <\/jats:italic>\n                      mice spontaneously recapitulated aspects of inflammatory challenges, including lung-predominant vascular hyperpermeability, immune cell recruitment, and fibrosis. These phenotypes were associated with a lung-specific decrease in the expression of\n                      <jats:italic toggle=\"yes\">Tek<\/jats:italic>\n                      \u2014a gene target of ERG previously implicated in maintaining pulmonary vascular stability during inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Collectively, our data highlight a unique role for ERG in pulmonary vascular function. We propose that cytokine-induced ERG degradation and subsequent transcriptional changes in lung ECs play critical roles in the destabilization of pulmonary blood vessels during infectious diseases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.123.318926","type":"journal-article","created":{"date-parts":[[2023,6,15]],"date-time":"2023-06-15T05:00:21Z","timestamp":1686805221000},"page":"1412-1428","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":26,"title":["Cytokine-Mediated Degradation of the Transcription Factor ERG Impacts the Pulmonary Vascular Response to Systemic Inflammatory Challenge"],"prefix":"10.1161","volume":"43","author":[{"given":"Christopher M.","family":"Schafer","sequence":"first","affiliation":[{"name":"Cardiovascular Biology Research Program (C.M.S., K.K., M.-L.W., C.F.J., A.B., E.W., K.W., A.C., C.T.G.), Oklahoma Medical Research 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