TXNIP deficiency exacerbates endotoxic shock via the induction of excessive nitric oxide synthesis

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dc.contributor.authorYoung-Jun Park-
dc.contributor.authorSung Jin Yoon-
dc.contributor.authorHyun Woo Suh-
dc.contributor.authorDongoh Kim-
dc.contributor.authorJ R Park-
dc.contributor.authorHaiyoung Jung-
dc.contributor.authorTae-Don Kim-
dc.contributor.authorSuk Ran Yoon-
dc.contributor.authorJeong Ki Min-
dc.contributor.authorHee-Jun Na-
dc.contributor.authorSeon-Jin Lee-
dc.contributor.authorHee Gu Lee-
dc.contributor.authorY H Lee-
dc.contributor.authorH B Lee-
dc.contributor.authorIn Pyo Choi-
dc.date.accessioned2017-04-19T09:43:42Z-
dc.date.available2017-04-19T09:43:42Z-
dc.date.issued2013-
dc.identifier.issn1553-7366-
dc.identifier.uri10.1371/journal.ppat.1003646ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11537-
dc.description.abstractThioredoxin-interacting protein (TXNIP) has multiple functions, including tumor suppression and involvement in cell proliferation and apoptosis. However, its role in the inflammatory process remains unclear. In this report, we demonstrate that Txnip-/- mice are significantly more susceptible to lipopolysaccharide (LPS)-induced endotoxic shock. In response to LPS, Txnip-/- macrophages produced significantly higher levels of nitric oxide (NO) and inducible nitric oxide synthase (iNOS), and an iNOS inhibitor rescued Txnip-/- mice from endotoxic shock-induced death, demonstrating that NO is a major factor in TXNIP-mediated endotoxic shock. This susceptibility phenotype of Txnip-/- mice occurred despite reduced IL-1β secretion due to increased S-nitrosylation of NLRP3 compared to wild-type controls. Taken together, these data demonstrate that TXNIP is a novel molecule that links NO synthesis and NLRP3 inflammasome activation during endotoxic shock.-
dc.publisherPublic Library of Science-
dc.titleTXNIP deficiency exacerbates endotoxic shock via the induction of excessive nitric oxide synthesis-
dc.title.alternativeTXNIP deficiency exacerbates endotoxic shock via the induction of excessive nitric oxide synthesis-
dc.typeArticle-
dc.citation.titlePLoS Pathogens-
dc.citation.number10-
dc.citation.endPage1003646-
dc.citation.startPage1003646-
dc.citation.volume9-
dc.contributor.affiliatedAuthorYoung-Jun Park-
dc.contributor.affiliatedAuthorSung Jin Yoon-
dc.contributor.affiliatedAuthorHyun Woo Suh-
dc.contributor.affiliatedAuthorDongoh Kim-
dc.contributor.affiliatedAuthorHaiyoung Jung-
dc.contributor.affiliatedAuthorTae-Don Kim-
dc.contributor.affiliatedAuthorSuk Ran Yoon-
dc.contributor.affiliatedAuthorJeong Ki Min-
dc.contributor.affiliatedAuthorHee-Jun Na-
dc.contributor.affiliatedAuthorSeon-Jin Lee-
dc.contributor.affiliatedAuthorHee Gu Lee-
dc.contributor.affiliatedAuthorIn Pyo Choi-
dc.contributor.alternativeName박영준-
dc.contributor.alternativeName윤성진-
dc.contributor.alternativeName서현우-
dc.contributor.alternativeName김동오-
dc.contributor.alternativeName박정란-
dc.contributor.alternativeName정해용-
dc.contributor.alternativeName김태돈-
dc.contributor.alternativeName윤석란-
dc.contributor.alternativeName민정기-
dc.contributor.alternativeName나희준-
dc.contributor.alternativeName이선진-
dc.contributor.alternativeName이희구-
dc.contributor.alternativeName이영호-
dc.contributor.alternativeName이희봉-
dc.contributor.alternativeName최인표-
dc.identifier.bibliographicCitationPLoS Pathogens, vol. 9, no. 10, pp. 1003646-1003646-
dc.identifier.doi10.1371/journal.ppat.1003646-
dc.description.journalClassY-
Appears in Collections:
Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
Aging Convergence Research Center > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Division of Biomedical Research > Biotherapeutics Translational Research Center > 1. Journal Articles
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