title: HMGB1 in the pathogenesis of ultraviolet-induced ocular surface inflammation.
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.
authors: Department of Ophthalmology, Institute of Vision Research, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
authors: S J
authors: SJ
authors: Han
authors: Department of Otorhinolaryngology - Head and Neck Surgery, Chung-Ang University College of Medicine, Seoul, Korea.|Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.
authors: H J
authors: HJ
authors: Min
authors: Department of Ophthalmology, Institute of Vision Research, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
authors: S C
authors: SC
authors: Yoon
authors: Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.|Department of Microbiology, Yonsei University College of Medicine, Seoul, Korea.
authors: E A
authors: EA
authors: Ko
authors: Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.|Department of Microbiology, Yonsei University College of Medicine, Seoul, Korea.
authors: S J
authors: SJ
authors: Park
authors: Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.|Department of Otorhinolaryngology, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.|Severance Biomedical Science Institute and Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Korea.
authors: J-H
authors: JH
authors: Yoon
authors: Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.|Department of Microbiology, Yonsei University College of Medicine, Seoul, Korea.|Severance Biomedical Science Institute and Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Korea.
authors: J-S
authors: JS
authors: Shin
authors: Department of Ophthalmology, Institute of Vision Research, Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
authors: K Y
authors: KY
authors: Seo
mesh_terms: D000818:Animals; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism / Q000528:radiation effects; D003228:Conjunctiva / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects*; D003593:Cytoplasm / Q000378:metabolism / Q000528:radiation effects; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects*; D005260:Female; D015870:Gene Expression; D024243:HMGB1 Protein / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007249:Inflammation; D051379:Mice; D008807:Mice, Inbred BALB C; D021381:Protein Transport; D011625:Pterygium / Q000209:etiology / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D017382:Reactive Oxygen Species / Q000819:agonists / Q000378:metabolism*; D000067759:Receptor for Advanced Glycation End Products / Q000737:chemistry / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: C000593873:Ager protein, mouse; D024243:HMGB1 Protein; C582808:HMGB1 protein, mouse; D017382:Reactive Oxygen Species; D000067759:Receptor for Advanced Glycation End Products