{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T18:07:16Z","timestamp":1779127636603,"version":"3.51.4"},"reference-count":45,"publisher":"American Society for Clinical Investigation","issue":"20","license":[{"start":{"date-parts":[[2025,9,23]],"date-time":"2025-09-23T00:00:00Z","timestamp":1758585600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"NIH","award":["P01 AI120944"],"award-info":[{"award-number":["P01 AI120944"]}]},{"name":"NIH","award":["R01 DK062357"],"award-info":[{"award-number":["R01 DK062357"]}]},{"name":"NIH","award":["R01 AI155856"],"award-info":[{"award-number":["R01 AI155856"]}]},{"DOI":"10.13039\/100016206","name":"UCLA Clinical and Translational Science Institute","doi-asserted-by":"crossref","award":["UL1TR001881"],"award-info":[{"award-number":["UL1TR001881"]}],"id":[{"id":"10.13039\/100016206","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/100023581","name":"National Science Foundation Graduate Research Fellowship Program","doi-asserted-by":"crossref","award":["No. DGE-2034835"],"award-info":[{"award-number":["No. DGE-2034835"]}],"id":[{"id":"10.13039\/100023581","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,9,23]]},"abstract":"<jats:p>\n                    Hepatic ischemia-reperfusion injury (IRI) disrupts cellular signaling pathways and contributes to early allograft dysfunction (EAD) in orthotopic liver transplantation (OLT). In this study, we found that the hepatic RNA binding protein Human Antigen R (HuR) regulated the 3\u2032 untranslated region (UTR) of Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 (\n                    <jats:italic>Ceacam1<\/jats:italic>\n                    ) following ischemic stress. Hepatocyte-specific preinjury HuR-null mice exhibited elevated LDH-5 isoenzyme activity and reduced Ceacam1-S expression, reflecting tissue-specific injury. In situ hybridization demonstrated that the stability of\n                    <jats:italic>Ceacam1<\/jats:italic>\n                    mRNA depended on HuR. Luciferase assays identified\n                    <jats:italic>Ceacam1<\/jats:italic>\n                    3\u2032UTR\n                    <jats:italic>cis<\/jats:italic>\n                    -elements responsive to high oxygen tension. HuR-targeting short-activating RNAs (saRNAs) preferentially induced the alternative splicing of\n                    <jats:italic>Ceacam1-S<\/jats:italic>\n                    . Antisense oligos directed to the Ceacam1 3\u2032UTR protected WT mice against acute liver injury. In the clinical arm, increased HuR and CEACAM1 expression were associated with reduced proinflammatory phenotype and a lower incidence of EAD in patients with OLT (\n                    <jats:italic>n<\/jats:italic>\n                    = 164). Human discarded livers with elevated\n                    <jats:italic>ELAVL1<\/jats:italic>\n                    \/\n                    <jats:italic>CEACAM1<\/jats:italic>\n                    levels correlated with improved tissue homeostasis. These findings suggest that HuR regulation of Ceacam1 represents a key determinant of donor tissue quality and offers a potential target for future therapeutic strategies in OLT recipients.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.194227","type":"journal-article","created":{"date-parts":[[2025,9,22]],"date-time":"2025-09-22T18:00:46Z","timestamp":1758564046000},"source":"Crossref","is-referenced-by-count":0,"title":["Posttranscriptional control of hepatic CEACAM1 3\u2032UTR by human antigen R (HuR) mitigates sterile liver inflammation"],"prefix":"10.1172","volume":"10","author":[{"given":"Brian","family":"Cheng","sequence":"first","affiliation":[{"name":"The Dumont-UCLA Transplantation Center, Department of Surgery, Division of Liver and Pancreas Transplantation, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0684-8304","authenticated-orcid":true,"given":"Tristan 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and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Taylor","family":"Torgerson","sequence":"additional","affiliation":[{"name":"The Dumont-UCLA Transplantation Center, Department of Surgery, Division of Liver and Pancreas Transplantation, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard","family":"Chiu","sequence":"additional","affiliation":[{"name":"The Dumont-UCLA Transplantation Center, Department of Surgery, Division of Liver and Pancreas Transplantation, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aanchal S.","family":"Kasargod","sequence":"additional","affiliation":[{"name":"The Dumont-UCLA Transplantation Center, Department of Surgery, Division of Liver and Pancreas Transplantation, and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kojiro","family":"Nakamura","sequence":"additional","affiliation":[{"name":"The Dumont-UCLA Transplantation Center, Department of Surgery, Division of Liver and 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