Matches in UGent Biblio for { <https://biblio.ugent.be/publication/1078689#aggregation> ?p ?o. }
Showing items 1 to 42 of
42
with 100 items per page.
- aggregation classification "A1".
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2010".
- aggregation format "application/pdf".
- aggregation hasFormat 1078689.bibtex.
- aggregation hasFormat 1078689.csv.
- aggregation hasFormat 1078689.dc.
- aggregation hasFormat 1078689.didl.
- aggregation hasFormat 1078689.doc.
- aggregation hasFormat 1078689.json.
- aggregation hasFormat 1078689.mets.
- aggregation hasFormat 1078689.mods.
- aggregation hasFormat 1078689.rdf.
- aggregation hasFormat 1078689.ris.
- aggregation hasFormat 1078689.txt.
- aggregation hasFormat 1078689.xls.
- aggregation hasFormat 1078689.yaml.
- aggregation isPartOf urn:issn:0022-1767.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Medicine and Health Sciences".
- aggregation title "Hydroxylase inhibition abrogates TNF-α-induced intestinal epithelial damage by hypoxia-inducible factor-1-dependent repression of FADD".
- aggregation abstract "Hydroxylase inhibitors stabilize hypoxia-inducible factor-1 (HIF-1), which has barrier-protective activity in the gut. Because the inflammatory cytokine TNF-a contributes to inflammatory bowel disease in part by compromising intestinal epithelial barrier integrity, hydroxylase inhibition may have beneficial effects in TNF-a–induced intestinal epithelial damage. The hydroxylase inhibitor dimethyloxalylglycin (DMOG) was tested in a murine model of TNF-a–driven chronic terminal ileitis. DMOG-treated mice experienced clinical benefit and showed clear attenuation of chronic intestinal inflammation compared with that of vehicle-treated littermates. Additional in vivo and in vitro experiments revealed that DMOG rapidly restored terminal ileal barrier function, at least in part through prevention of TNF-a–induced intestinal epithelial cell apoptosis. Subsequent transcriptional studies indicated that DMOG repressed Fas-associated death domain protein (FADD), a critical adaptor molecule in TNFR-1- mediated apoptosis, in an HIF-1a–dependent manner. Loss of this FADD repression by HIF-1a-targeting small interfering RNA significantly diminished the antiapoptotic action of DMOG. Additional molecular studies led to the discovery of a previously unappreciated HIF-1 binding site in the FADD promoter, which controls repression of FADD during hypoxia. As such, the results reported in this study allowed the identification of an innate mechanism that protects intestinal epithelial cells during (inflammatory) hypoxia, by direct modulation of death receptor signaling. Hydroxylase inhibition could represent a promising alternative treatment strategy for hypoxic inflammatory diseases, including inflammatory bowel disease.".
- aggregation authorList BK846868.
- aggregation endPage "6316".
- aggregation issue "10".
- aggregation startPage "6306".
- aggregation volume "185".
- aggregation aggregates 2937567.
- aggregation isDescribedBy 1078689.
- aggregation similarTo jimmunol.1002541.
- aggregation similarTo LU-1078689.