Hosoon Choi1, Casie Phillips1, Joo Youn Oh2, Eileen M Stock3, Dong-Ki Kim4, Jae-Kyung Won5, Samuel Fulcher6. 1. a Department of Basic Research , Central Texas Veterans Research Foundation , Temple , TX , USA. 2. b Department of Ophthalmology , Seoul National University Hospital, Daehak-ro, Jongno-gu , Seoul , Republic of Korea. 3. c Cooperative Studies Program Coordinating Center , VA Maryland Health Care System , Perry Point , MD , USA. 4. d Institute for Regenerative Medicine, Texas A&M Health Science Center, College Station , TX , USA. 5. e Department of Pathology, Seoul National University Hospital , Daehak-ro, Jongno-gu , Seoul , Republic of Korea. 6. f Department of Surgery, Ophthalmology Section , Central Texas Veterans Health Care System , Temple , TX , USA.
Abstract
PURPOSE: To characterize the molecular, clinical, and histopathological profiles in the rat cornea after alkali injury over a 21-day period. METHODS: Alkali injury was induced in one eye of male Lewis rats. Corneal opacity and corneal neovascularization were assessed daily. Real-time qRT-PCR analysis and immunohistochemical staining were conducted to examine inflammation, neovascularization, and fibrosis. RESULTS: We found that within 2 hours of chemical exposure, corneal opacification rapidly developed with an acute increase in various cytokine expressions, while several cytokines demonstrated a secondary peak by day 7. Early neutrophil infiltration peaked at day 1 post-injury while macrophage infiltration peaked at day 7. Throughout the time course of the study, corneal opacity persisted and neovascularization, lymphangiogenesis, and fibrosis progressed. CONCLUSIONS: This study highlights the molecular, clinical, and histopathological changes throughout the progression of alkali injury in the rat cornea. These profiles will assist in the development of new strategies and therapies for ocular alkali injury.
PURPOSE: To characterize the molecular, clinical, and histopathological profiles in the rat cornea after alkali injury over a 21-day period. METHODS:Alkali injury was induced in one eye of male Lewis rats. Corneal opacity and corneal neovascularization were assessed daily. Real-time qRT-PCR analysis and immunohistochemical staining were conducted to examine inflammation, neovascularization, and fibrosis. RESULTS: We found that within 2 hours of chemical exposure, corneal opacification rapidly developed with an acute increase in various cytokine expressions, while several cytokines demonstrated a secondary peak by day 7. Early neutrophil infiltration peaked at day 1 post-injury while macrophage infiltration peaked at day 7. Throughout the time course of the study, corneal opacity persisted and neovascularization, lymphangiogenesis, and fibrosis progressed. CONCLUSIONS: This study highlights the molecular, clinical, and histopathological changes throughout the progression of alkali injury in the rat cornea. These profiles will assist in the development of new strategies and therapies for ocular alkali injury.
Authors: Jonathan Luisi; Edward R Kraft; Steven A Giannos; Krishna Patel; Mary E Schmitz-Brown; Valentina Reffatto; Kevin H Merkley; Praveena K Gupta Journal: Transl Vis Sci Technol Date: 2021-03-01 Impact factor: 3.283