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HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation
by
Park, S J
, Han, S J
, Min, H J
, Ko, E A
, Shin, J-S
, Yoon, S C
, Yoon, J-H
, Seo, K Y
in
14/19
/ 14/63
/ 38/109
/ 42/34
/ 631/45/612/822
/ 64/60
/ 692/420
/ 692/699/3161
/ 692/700/565/1436/2185
/ 82/51
/ Animals
/ Antibodies
/ Biochemistry
/ Biomedical and Life Sciences
/ Cell Biology
/ Cell Culture
/ Cell Line
/ Cell Nucleus - metabolism
/ Cell Nucleus - radiation effects
/ Conjunctiva - metabolism
/ Conjunctiva - pathology
/ Conjunctiva - radiation effects
/ Cytoplasm - metabolism
/ Cytoplasm - radiation effects
/ Epithelial Cells - metabolism
/ Epithelial Cells - pathology
/ Epithelial Cells - radiation effects
/ Female
/ Gene Expression
/ HMGB1 Protein - genetics
/ HMGB1 Protein - metabolism
/ Humans
/ Immunology
/ Inflammation
/ Life Sciences
/ Mice
/ Mice, Inbred BALB C
/ Original
/ original-article
/ Protein Transport
/ Pterygium - etiology
/ Pterygium - genetics
/ Pterygium - metabolism
/ Pterygium - pathology
/ Reactive Oxygen Species - agonists
/ Reactive Oxygen Species - metabolism
/ Receptor for Advanced Glycation End Products - chemistry
/ Receptor for Advanced Glycation End Products - genetics
/ Receptor for Advanced Glycation End Products - metabolism
/ Signal Transduction
/ Ultraviolet Rays - adverse effects
2015
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HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation
by
Park, S J
, Han, S J
, Min, H J
, Ko, E A
, Shin, J-S
, Yoon, S C
, Yoon, J-H
, Seo, K Y
in
14/19
/ 14/63
/ 38/109
/ 42/34
/ 631/45/612/822
/ 64/60
/ 692/420
/ 692/699/3161
/ 692/700/565/1436/2185
/ 82/51
/ Animals
/ Antibodies
/ Biochemistry
/ Biomedical and Life Sciences
/ Cell Biology
/ Cell Culture
/ Cell Line
/ Cell Nucleus - metabolism
/ Cell Nucleus - radiation effects
/ Conjunctiva - metabolism
/ Conjunctiva - pathology
/ Conjunctiva - radiation effects
/ Cytoplasm - metabolism
/ Cytoplasm - radiation effects
/ Epithelial Cells - metabolism
/ Epithelial Cells - pathology
/ Epithelial Cells - radiation effects
/ Female
/ Gene Expression
/ HMGB1 Protein - genetics
/ HMGB1 Protein - metabolism
/ Humans
/ Immunology
/ Inflammation
/ Life Sciences
/ Mice
/ Mice, Inbred BALB C
/ Original
/ original-article
/ Protein Transport
/ Pterygium - etiology
/ Pterygium - genetics
/ Pterygium - metabolism
/ Pterygium - pathology
/ Reactive Oxygen Species - agonists
/ Reactive Oxygen Species - metabolism
/ Receptor for Advanced Glycation End Products - chemistry
/ Receptor for Advanced Glycation End Products - genetics
/ Receptor for Advanced Glycation End Products - metabolism
/ Signal Transduction
/ Ultraviolet Rays - adverse effects
2015
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HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation
by
Park, S J
, Han, S J
, Min, H J
, Ko, E A
, Shin, J-S
, Yoon, S C
, Yoon, J-H
, Seo, K Y
in
14/19
/ 14/63
/ 38/109
/ 42/34
/ 631/45/612/822
/ 64/60
/ 692/420
/ 692/699/3161
/ 692/700/565/1436/2185
/ 82/51
/ Animals
/ Antibodies
/ Biochemistry
/ Biomedical and Life Sciences
/ Cell Biology
/ Cell Culture
/ Cell Line
/ Cell Nucleus - metabolism
/ Cell Nucleus - radiation effects
/ Conjunctiva - metabolism
/ Conjunctiva - pathology
/ Conjunctiva - radiation effects
/ Cytoplasm - metabolism
/ Cytoplasm - radiation effects
/ Epithelial Cells - metabolism
/ Epithelial Cells - pathology
/ Epithelial Cells - radiation effects
/ Female
/ Gene Expression
/ HMGB1 Protein - genetics
/ HMGB1 Protein - metabolism
/ Humans
/ Immunology
/ Inflammation
/ Life Sciences
/ Mice
/ Mice, Inbred BALB C
/ Original
/ original-article
/ Protein Transport
/ Pterygium - etiology
/ Pterygium - genetics
/ Pterygium - metabolism
/ Pterygium - pathology
/ Reactive Oxygen Species - agonists
/ Reactive Oxygen Species - metabolism
/ Receptor for Advanced Glycation End Products - chemistry
/ Receptor for Advanced Glycation End Products - genetics
/ Receptor for Advanced Glycation End Products - metabolism
/ Signal Transduction
/ Ultraviolet Rays - adverse effects
2015
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HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation
Journal Article
HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation
2015
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Overview
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.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
/ 14/63
/ 38/109
/ 42/34
/ 64/60
/ 692/420
/ 82/51
/ Animals
/ Biomedical and Life Sciences
/ Cell Nucleus - radiation effects
/ Conjunctiva - radiation effects
/ Cytoplasm - radiation effects
/ Epithelial Cells - metabolism
/ Epithelial Cells - pathology
/ Epithelial Cells - radiation effects
/ Female
/ Humans
/ Mice
/ Original
/ Reactive Oxygen Species - agonists
/ Reactive Oxygen Species - metabolism
/ Receptor for Advanced Glycation End Products - chemistry
/ Receptor for Advanced Glycation End Products - genetics
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