HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation

S. J. Han; H. J. Min; S. C. Yoon; E. A. Ko; S. J. Park; J. H. Yoon; J. S. Shin; K. Y. Seo

doi:10.1038/cddis.2015.199

HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation

S. J. Han, H. J. Min, S. C. Yoon, E. A. Ko, S. J. Park, J. H. Yoon, J. S. Shin, K. Y. Seo

Department of Ophthalmology

Research output: Contribution to journal › Article › peer-review

20 Citations (Scopus)

Abstract

High-mobility group box 1 (HMGB1) functions as a transcription-enhancing nuclear protein as well as a crucial cytokine that regulates inflammation. This study demonstrated that secretion of HMGB1 due to ultraviolet (UV) radiation inducing ocular surface inflammation-mediated reactive oxygen species (ROS) production. After treating conjunctival epithelial cells with UV radiation, HMGB1 was translocated from the nucleus to the cytoplasm and then eventually to the extracellular space. HMGB1 played a crucial role in UV-induced conjunctival neutrophil infiltration, which subsided when mice were pretreated with the HMGB1 inhibitors soluble receptor for advanced glycation endproducts (sRAGEs) and HMGB1 A box protein. In case of using ROS quencher, there was decrease in UV-induced HMGB1 secretion in conjunctival epithelial cells and mice. Considering that UV-induced chronic inflammation causes ocular surface change as pterygium, we have confirmed high HMGB1 translocation and ROS expression in human pterygium. Our findings therefore revealed a previously unknown mechanism of UV-induced ocular inflammation related to ROS and HMGB1 suggesting a new medical therapeutic target.

Original language	English
Article number	e1863
Journal	Cell Death and Disease
Volume	6
Issue number	8
DOIs	https://doi.org/10.1038/cddis.2015.199
Publication status	Published - 2015 Aug 27

Bibliographical note

Funding Information:
Acknowledgements. This study was supported by grants from the National Research Foundation of Korea (NRF, MEST; No. 2011-0017611 and 2014R1A4A1008625), the Korea Healthcare Technology R&D Project (A121861), and the Korean Ministry for Health, Welfare and Family Affairs. The authors thank Dong-Su Jang (Yonsei University College of Medicine) for his help with the figures and Holden Yoon Seung Kim for critical reading.

Publisher Copyright:
© 2015 Macmillan Publishers Limited. All rights reserved.

All Science Journal Classification (ASJC) codes

Immunology
Cellular and Molecular Neuroscience
Cell Biology
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/cddis.2015.199

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abstract = "High-mobility group box 1 (HMGB1) functions as a transcription-enhancing nuclear protein as well as a crucial cytokine that regulates inflammation. This study demonstrated that secretion of HMGB1 due to ultraviolet (UV) radiation inducing ocular surface inflammation-mediated reactive oxygen species (ROS) production. After treating conjunctival epithelial cells with UV radiation, HMGB1 was translocated from the nucleus to the cytoplasm and then eventually to the extracellular space. HMGB1 played a crucial role in UV-induced conjunctival neutrophil infiltration, which subsided when mice were pretreated with the HMGB1 inhibitors soluble receptor for advanced glycation endproducts (sRAGEs) and HMGB1 A box protein. In case of using ROS quencher, there was decrease in UV-induced HMGB1 secretion in conjunctival epithelial cells and mice. Considering that UV-induced chronic inflammation causes ocular surface change as pterygium, we have confirmed high HMGB1 translocation and ROS expression in human pterygium. Our findings therefore revealed a previously unknown mechanism of UV-induced ocular inflammation related to ROS and HMGB1 suggesting a new medical therapeutic target.",

author = "Han, {S. J.} and Min, {H. J.} and Yoon, {S. C.} and Ko, {E. A.} and Park, {S. J.} and Yoon, {J. H.} and Shin, {J. S.} and Seo, {K. Y.}",

note = "Funding Information: Acknowledgements. This study was supported by grants from the National Research Foundation of Korea (NRF, MEST; No. 2011-0017611 and 2014R1A4A1008625), the Korea Healthcare Technology R&D Project (A121861), and the Korean Ministry for Health, Welfare and Family Affairs. The authors thank Dong-Su Jang (Yonsei University College of Medicine) for his help with the figures and Holden Yoon Seung Kim for critical reading. Publisher Copyright: {\textcopyright} 2015 Macmillan Publishers Limited. All rights reserved.",

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HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

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