{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T08:41:32Z","timestamp":1792658492743,"version":"4.5.0"},"reference-count":60,"publisher":"Bioscientifica","issue":"1","funder":[{"name":"National Institutes of Health","award":["R01DK088139, R01HD093701, R01HD107700"],"award-info":[{"award-number":["R01DK088139, R01HD093701, R01HD107700"]}]}],"content-domain":{"domain":["journals.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Diabetes results from an inflammatory insult to the pancreas. NF\u03baB is a key transcription factor regulating cellular inflammatory responses. Therefore, we hypothesized that inflammatory exposures would acutely activate NF\u03baB in the adult mouse pancreas and in isolated islets, leading to upregulation of target genes associated with inflammation and apoptosis. Mice were exposed to lipopolysaccharide (LPS), and isolated islets were exposed to a cytokine mixture to model a strong pro-inflammatory challenge. NF\u03baB activation was determined by phosphorylation and nuclear translocation of NF\u03baB proteins p65 and p50, dynamics of the inhibitors, I\u03baB\u03b1 and I\u03baB\u03b2, and the expression of NF\u03baB target genes. NF\u03baB target gene transcription was then correlated with p65 binding at promoter regions. Targeted apoptotic transcriptome changes were also evaluated. Systemic LPS exposure induced pancreatic NF\u03baB activation, as evidenced by I\u03baB oscillations and nuclear translocation of NF\u03baB subunits. In isolated islets, cytokines triggered rapid p65 phosphorylation and DNA binding and increased NF\u03baB target gene expression, with corresponding increases in specific promoter binding. Notably, anti-apoptotic genes were upregulated. These findings demonstrate that acute inflammatory stress activates NF\u03baB in pancreatic tissue and islets, promoting a pro-inflammatory yet anti-apoptotic transcriptional response. Targeting NF\u03baB at specific time points after inflammation may help prevent \u03b2-cell injury and diabetes development.<\/jats:p>","DOI":"10.1530\/joe-26-0138","type":"journal-article","created":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T13:52:03Z","timestamp":1791467523000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-5","source":"Crossref","is-referenced-by-count":0,"title":["Inflammation-induced NF\u03baB activation drives a pro-inflammatory and anti-apoptotic transcriptome in mouse islets"],"prefix":"10.1530","volume":"271","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1829-8346","authenticated-orcid":true,"given":"Alicia","family":"White","sequence":"first","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Department of Pediatrics 1 , , ,","place":["Aurora, Colorado, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mack","family":"Solar","sequence":"additional","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Department of Pediatrics 1 , , ,","place":["Aurora, Colorado, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenneth L","family":"Jones","sequence":"additional","affiliation":[{"name":"Bioinformatics Solutions 2 , , ,","place":["Sheridan, Wyoming, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natarajan","family":"Balasubramaniyan","sequence":"additional","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Department of Pediatrics 1 , , ,","place":["Aurora, Colorado, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul J","family":"Rozance","sequence":"additional","affiliation":[{"name":"University of Colorado Anschutz Medical Campus, Department of Pediatrics 1 , , ,","place":["Aurora, Colorado, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clyde J","family":"Wright","sequence":"additional","affiliation":[{"name":"University of Colorado 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