Hepatocyte DAX1 deletion exacerbates inflammatory liver injury by inducing the recruitment of CD4+ and CD8+ T cells through NF-κB p65 signaling pathway in mice

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dc.contributor.authorHyo Jeong Yun-
dc.contributor.authorYoung Joo Suh-
dc.contributor.authorYu-Bin Kim-
dc.contributor.authorEun Jung Kang-
dc.contributor.authorJung-Hyeon Choi-
dc.contributor.authorYoung Keun Choi-
dc.contributor.authorIn-Bok Lee-
dc.contributor.authorDong Hee Choi-
dc.contributor.authorYun Jeong Seo-
dc.contributor.authorJung Ran Noh-
dc.contributor.authorH S Choi-
dc.contributor.authorYong-Hoon Kim-
dc.contributor.authorChul-Ho Lee-
dc.date.accessioned2022-11-21T16:32:32Z-
dc.date.available2022-11-21T16:32:32Z-
dc.date.issued2022-
dc.identifier.issn1661-6596-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/30620-
dc.description.abstractFulminant hepatitis is characterized by rapid and massive immune-mediated liver injury. Dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome, gene 1 (DAX1; NR0B1) represses the transcription of various genes. Here, we determine whether DAX1 serves as a regulator of inflammatory liver injury induced by concanavalin A (ConA). C57BL/6J (WT), myeloid cell-specific Dax1 knockout (MKO), and hepatocyte-specific Dax1 knockout (LKO) mice received single intravenous administration of ConA. Histopathological changes in liver and plasma alanine aminotransferase and aspartate aminotransferase levels in Dax1 MKO mice were comparable with those in WT mice following ConA administration. Unlike Dax1 MKO mice, Dax1 LKO mice were greatly susceptible to ConA-induced liver injury, which was accompanied by enhanced infiltration of immune cells, particularly CD4+ and CD8+ T cells, in the liver. Factors related to T-cell recruitment, including chemokines and adhesion molecules, significantly increased following enhanced and prolonged phosphorylation of NF-κB p65 in the liver of ConA-administered Dax1 LKO mice. This is the first study to demonstrate that hepatocyte-specific DAX1 deficiency exacerbates inflammatory liver injury via NF-κB p65 activation, thereby causing T-cell infiltration by modulating inflammatory chemokines and adhesion molecules. Our results suggest DAX1 as a therapeutic target for fulminant hepatitis treatment.-
dc.publisherMDPI-
dc.titleHepatocyte DAX1 deletion exacerbates inflammatory liver injury by inducing the recruitment of CD4+ and CD8+ T cells through NF-κB p65 signaling pathway in mice-
dc.title.alternativeHepatocyte DAX1 deletion exacerbates inflammatory liver injury by inducing the recruitment of CD4+ and CD8+ T cells through NF-κB p65 signaling pathway in mice-
dc.typeArticle-
dc.citation.titleInternational Journal of Molecular Sciences-
dc.citation.number22-
dc.citation.endPage14009-
dc.citation.startPage14009-
dc.citation.volume23-
dc.contributor.affiliatedAuthorHyo Jeong Yun-
dc.contributor.affiliatedAuthorYoung Joo Suh-
dc.contributor.affiliatedAuthorYu-Bin Kim-
dc.contributor.affiliatedAuthorEun Jung Kang-
dc.contributor.affiliatedAuthorJung-Hyeon Choi-
dc.contributor.affiliatedAuthorYoung Keun Choi-
dc.contributor.affiliatedAuthorIn-Bok Lee-
dc.contributor.affiliatedAuthorDong Hee Choi-
dc.contributor.affiliatedAuthorYun Jeong Seo-
dc.contributor.affiliatedAuthorJung Ran Noh-
dc.contributor.affiliatedAuthorYong-Hoon Kim-
dc.contributor.affiliatedAuthorChul-Ho Lee-
dc.contributor.alternativeName윤효정-
dc.contributor.alternativeName서영주-
dc.contributor.alternativeName김유빈-
dc.contributor.alternativeName강은정-
dc.contributor.alternativeName최정현-
dc.contributor.alternativeName최영근-
dc.contributor.alternativeName이인복-
dc.contributor.alternativeName최동희-
dc.contributor.alternativeName서윤정-
dc.contributor.alternativeName노정란-
dc.contributor.alternativeName최흥식-
dc.contributor.alternativeName김용훈-
dc.contributor.alternativeName이철호-
dc.identifier.bibliographicCitationInternational Journal of Molecular Sciences, vol. 23, no. 22, pp. 14009-14009-
dc.identifier.doi10.3390/ijms232214009-
dc.subject.keywordCncanavalin A-
dc.subject.keywordDAX1-
dc.subject.keywordInflammatory liver injury-
dc.subject.keywordNF-kB-
dc.subject.keywordT cell-
dc.subject.localDAX1-
dc.subject.localNFkappaB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNf-κb-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localNuclear factor kappaB-
dc.subject.localNuclear factor κB-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor-kappa B-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localNuclear factor-κB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-kB-
dc.subject.localNF-kappa B-
dc.subject.localNF-kappaB-
dc.subject.localNF-ΚB-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localnuclear factor kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localnuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localT cell-
dc.subject.localT cells-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
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