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Your search keyword '"Shunsuke Kubota"' showing total 2 results
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2 results on '"Shunsuke Kubota"'

1. Hydrogen and N-acetyl-L-cysteine rescue oxidative stress-induced angiogenesis in a mouse corneal alkali-burn model

Author

Kazuo Tsubota, Miyuki Kubota, Yoko Ozawa, Shigeto Shimmura, Shunsuke Kubota, Kousuke Noda, Kazuo Umezawa, Naoko Kato, Toshihide Kurihara, Hideyuki Miyashita, Susumu Ishida, and Tomohiko Usui

Subjects
CD31, Male, Vascular Endothelial Growth Factor A, Pathology, medicine.medical_specialty, Antioxidant, Angiogenesis, medicine.medical_treatment, Enzyme-Linked Immunosorbent Assay, Pharmacology, medicine.disease_cause, Blindness, Antioxidants, chemistry.chemical_compound, Mice, Superoxide Dismutase-1, Downregulation and upregulation, Cornea, Burns, Chemical, medicine, Animals, Sodium Hydroxide, Corneal Neovascularization, Deuterium Oxide, Chemokine CCL2, chemistry.chemical_classification, Mice, Knockout, Reactive oxygen species, Mice, Inbred ICR, Cyclohexanones, Reverse Transcriptase Polymerase Chain Reaction, Superoxide Dismutase, NF-kappa B, Acetylcysteine, Vascular endothelial growth factor, Disease Models, Animal, Eye Burns, Oxidative Stress, medicine.anatomical_structure, chemistry, Microscopy, Fluorescence, Benzamides, Reactive Oxygen Species, Oxidative stress
Abstract

PURPOSE To investigate the role of reactive oxygen species (ROS) as the prime initiators of the angiogenic response after alkali injury of the cornea and observe the effects of antioxidants in preventing angiogenesis. METHODS The corneal epithelia of SOD-1-deficient mice or wild-type (WT) mice were removed after application of 0.15 N NaOH to establish the animal model of alkali burn. ROS production was semiquantitatively measured by dihydroethidium (DHE) fluorescence. Angiogenesis was visualized by CD31 immunohistochemistry. The effects of the specific NF-κB inhibitor DHMEQ, the antioxidant N-acetyl-L-cysteine (NAC), and hydrogen (H2) solution were observed. RESULTS ROS production in the cornea was enhanced immediately after alkali injury, as shown by increased DHE fluorescence (P

Published
2010

2. SARM1 depletion rescues NMNAT1-dependent photoreceptor cell death and retinal degeneration.

Author

Yo Sasaki, Hiroki Kakita, Shunsuke Kubota, Sene, Abdoulaye, Tae Jun Lee, Norimitsu Ban, Zhenyu Dong, Lin, Joseph B., Boye, Sanford L., DiAntonio, Aaron, Boye, Shannon E., Apte, Rajendra S., and Milbrandt, Jeffrey

Subjects
*PHOTORECEPTORS, *RETINAL degeneration, *CELL death, *VISION disorders, *ADULTS, *BLINDNESS
Abstract

Leber congenital amaurosis type nine is an autosomal recessive retinopathy caused by mutations of the NAD+ synthesis enzyme NMNAT1. Despite the ubiquitous expression of NMNAT1, patients do not manifest pathologies other than retinal degeneration. Here we demonstrate that widespread NMNAT1 depletion in adult mice mirrors the human pathology, with selective loss of photoreceptors highlighting the exquisite vulnerability of these cells to NMNAT1 loss. Conditional deletion demonstrates that NMNAT1 is required within the photoreceptor. Mechanistically, loss of NMNAT1 activates the NADase SARM1, the central executioner of axon degeneration, to trigger photoreceptor death and vision loss. Hence, the essential function of NMNAT1 in photoreceptors is to inhibit SARM1, highlighting an unexpected shared mechanism between axonal degeneration and photoreceptor neurodegeneration. These results define a novel SARM1-dependent photoreceptor cell death pathway and identifies SARM1 as a therapeutic candidate for retinopathies. [ABSTRACT FROM AUTHOR]

Published
2020
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