Literature DB >> 32426849

Disulfide High-Mobility Group Box 1 Drives Ischemia-Reperfusion Injury in Human Liver Transplantation.

Rebecca A Sosa1, Allyson Q Terry1, Fady M Kaldas2, Yi-Ping Jin1, Maura Rossetti1, Takahiro Ito2, Fang Li1, Richard S Ahn3, Bita V Naini1, Victoria M Groysberg1, Ying Zheng1, Antony Aziz2, Jessica Nevarez-Mejia1, Ali Zarrinpar2, Ronald W Busuttil2, David W Gjertson1,4, Jerzy W Kupiec-Weglinski1,2, Elaine F Reed1.   

Abstract

BACKGROUND AND AIMS: Sterile inflammation is a major clinical concern during ischemia-reperfusion injury (IRI) triggered by traumatic events, including stroke, myocardial infarction, and solid organ transplantation. Despite high-mobility group box 1 (HMGB1) clearly being involved in sterile inflammation, its role is controversial because of a paucity of patient-focused research. APPROACH AND
RESULTS: Here, we examined the role of HMGB1 oxidation states in human IRI following liver transplantation. Portal blood immediately following allograft reperfusion (liver flush; LF) had increased total HMGB1, but only LF from patients with histopathological IRI had increased disulfide-HMGB1 and induced Toll-like receptor 4-dependent tumor necrosis factor alpha production by macrophages. Disulfide HMGB1 levels increased concomitantly with IRI severity. IRI+ prereperfusion biopsies contained macrophages with hyperacetylated, lysosomal disulfide-HMGB1 that increased postreperfusion at sites of injury, paralleling increased histone acetyltransferase general transcription factor IIIC subunit 4 and decreased histone deacetylase 5 expression. Purified disulfide-HMGB1 or IRI+ blood stimulated further production of disulfide-HMGB1 and increased proinflammatory molecule and cytokine expression in macrophages through a positive feedback loop.
CONCLUSIONS: These data identify disulfide-HMGB1 as a mechanistic biomarker of, and therapeutic target for, minimizing sterile inflammation during human liver IRI.
© 2020 by the American Association for the Study of Liver Diseases.

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Year:  2020        PMID: 32426849      PMCID: PMC8722704          DOI: 10.1002/hep.31324

Source DB:  PubMed          Journal:  Hepatology        ISSN: 0270-9139            Impact factor:   17.425


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