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286 results on '"Harada, Chikako"'

13. Vision protection and robust axon regeneration in glaucoma models by membrane-associated Trk receptors

Author

Nishijima, Euido, primary, Honda, Sari, additional, Kitamura, Yuta, additional, Namekata, Kazuhiko, additional, Kimura, Atsuko, additional, Guo, Xiaoli, additional, Azuchi, Yuriko, additional, Harada, Chikako, additional, Murakami, Akira, additional, Matsuda, Akira, additional, Nakano, Tadashi, additional, Parada, Luis F., additional, and Harada, Takayuki, additional

Published
2022
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14. Neurotrophic Factors

Author

Harada, Chikako, Harada, Takayuki, Nakazawa, Toru, editor, Kitaoka, Yasushi, editor, and Harada, Takayuki, editor

Published
2014
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21. Membrane-associated shortened Trk receptors promote neuroprotection and robust axon regeneration without ligands

Author

Nishijima, Euido, primary, Honda, Sari, additional, Kitamura, Yuta, additional, Namekata, Kazuhiko, additional, Kimura, Atsuko, additional, Guo, Xiaoli, additional, Azuchi, Yuriko, additional, Harada, Chikako, additional, Murakami, Akira, additional, Matsuda, Akira, additional, Nakano, Tadashi, additional, Parada, Luis F., additional, and Harada, Takayuki, additional

Published
2022
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27. The potential role of glutamate transporters in the pathogenesis of normal tension glaucoma

Author

Harada, Takayuki, Harada, Chikako, Nakamura, Kazuaki, Quah, Hun-Meng A., Okumura, Akinori, Namekata, Kazuhiko, Saeki, Tadashiro, Aihara, Makoto, Yoshida, Hiroshi, Mitani, Akira, and Tanaka, Kohichi

Subjects
Ganglion -- Health aspects, Glaucoma -- Risk factors, Glaucoma -- Diagnosis, Glaucoma -- Prevention, Glaucoma -- Research, Carrier proteins -- Health aspects
Abstract

Glaucoma, a progressive optic neuropathy due to retinal ganglion cell (RGC) degeneration, is one of the leading causes of irreversible blindness. Although glaucoma is often associated with elevated intraocular pressure [...]

Published
2007

28. Molecular regulation of visual system development: More than meets the eye

Author

Harada, Takayuki, Harada, Chikako, and Farada, Luis F.

Subjects
Eye -- Research, Developmental biology -- Research, Molecular biology -- Research, Biological sciences
Abstract

The progress on the molecular mechanisms underlying the development of the eye, visual system, and embryonic tumors that arise in the optic system is reviewed. The findings suggest that various genes affecting the relative positioning of thalamocortical (TC) axons within the subcortical telencephalon (ST) might modify the cortical area including the visual cortex.

Published
2007

29. Topical Ripasudil Suppresses Retinal Ganglion Cell Death in a Mouse Model of Normal Tension Glaucoma

Author

Akaiwa, Kei, Namekata, Kazuhiko, Azuchi, Yuriko, Sano, Hiroki, Guo, Xiaoli, Kimura, Atsuko, Harada, Chikako, Mitamura, Yoshinori, and Harada, Takayuki

Subjects
glaucoma, genetic structures, ripasudil, neuroprotection, p38, sense organs, eye diseases, intraocular pressure
Abstract

PURPOSE. To assess if ripasudil has a neuroprotective effect using mice with excitatory amino acid carrier 1 (EAAC1) deletion (EAAC1 knockout [KO] mice), a mouse model of normal tension glaucoma. METHODS. Topical administration (5 μL/day) of two different concentrations of ripasudil (0.4% and 2%) were applied to EAAC1 KO mice from 5 to 12 weeks old. Optical coherence tomography, multifocal electroretinograms, the measurement of intraocular pressure (IOP), and histopathology analyses were performed at 5, 8, and 12 weeks old. Retrograde labeling of retinal ganglion cells (RGCs), immunoblot, and immunohistochemical analyses of phosphorylated p38 mitogen-activated protein kinase (MAPK) in the retina were performed at 8 weeks old. RESULTS. Topical ripasudil ameliorated retinal degeneration and improved visual function in EAAC1 KO mice at both 8 and 12 weeks old. Ripasudil reduced IOP and strongly suppressed the phosphorylation of p38 MAPK that stimulates RGC death in EAAC1 KO mice. CONCLUSIONS. These results suggest that, in addition to IOP reduction, ripasudil prevents glaucomatous retinal degeneration by neuroprotection, which is achieved by suppressing cell-death signaling pathways.

Published
2018

30. Effect of p75.sup.NTR on the regulation of naturally occurring cell death and retinal ganglion cell number in the mouse eye

Author

Harada, Chikako, Harada, Takayuki, Nakamura, Kazuaki, Sakai, Yasuo, Tanaka, Kohichi, and Parada, Luis F.

Subjects
Cell death -- Analysis, Biochemistry -- Analysis, Developmental biology -- Analysis, Neurosciences -- Analysis, Transforming growth factors -- Analysis, Ganglion -- Analysis, Tyrosine -- Analysis, Nerve growth factor -- Analysis, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2005.08.051 Byline: Chikako Harada (a)(b)(c), Takayuki Harada (a)(b)(c), Kazuaki Nakamura (a), Yasuo Sakai (b), Kohichi Tanaka (c)(d), Luis F. Parada (b) Keywords: Eye development; Retina; Programmed cell death; Neurotrophins; p75.sup.NTR; TrkA; Retinal ganglion cell; Pax6; Mouse Abstract: Neurotrophins induce neural cell survival and differentiation during retinal development and regeneration through the high-affinity tyrosine kinase (Trk) receptors. On the other hand, nerve growth factor (NGF) binding to the low-affinity neurotrophin receptor p75 (p75.sup.NTR) might induce programmed cell death (PCD) in the early phase of retinal development. In the present study, we examined the retinal cell types that experience p75.sup.NTR-induced PCD and identify them to be postmitotic retinal ganglion cells (RGCs). However, retinal morphology, RGC number, and BrdU-positive cell number in p75.sup.NTR knockout (KO) mouse were normal after embryonic day 15 (E15). In chick retina, migratory RGCs express p75.sup.NTR, whereas layered RGCs express the high-affinity NGF receptor TrkA, which may switch the pro-apoptotic signaling of p75.sup.NTR into a neurotrophic one. In contrast to the chick model, migratory RGCs express TrkA, while stratified RGCs express p75.sup.NTR in mouse retina. However, RGC number in TrkA KO mouse was also normal at birth. We next examined the expression of transforming growth factor [beta] (TGF[beta]) receptor, which modulates chick RGC number in combination with p75.sup.NTR, but was absent in mouse RGCs. p75.sup.NTR and TrkA seem to be involved in the regulation of mouse RGC number in the early phase of retinal development, but the number may be later adjusted by other molecules. These results suggest the different mechanism of RGC number control between mouse and chick retina. Author Affiliation: (a) Department of Molecular Neurobiology, Tokyo Metropolitan Institute for Neuroscience, Fuchu, Tokyo 183-8526, Japan (b) Center for Developmental Biology and Kent Waldrep Foundation Center for Basic Research on Nerve Growth and Regeneration, University of Texas Southwestern Medical Center, Dallas, TX 75390-9133, USA (c) Laboratory of Molecular Neuroscience, School of Biomedical Science and Medical Research Institute, Tokyo Medical and Dental University, Tokyo 113-8510, Japan (d) PRESTO, Japan Science and Technology Corporation (JST), Kawaguchi, Saitama 332-0012, Japan Article History: Received 11 November 2003; Revised 20 July 2005; Accepted 4 August 2005

Published
2006

41. Normal tension glaucoma-like degeneration of the visual system in aged marmosets

Author

Noro, Takahiko, primary, Namekata, Kazuhiko, additional, Kimura, Atsuko, additional, Azuchi, Yuriko, additional, Hashimoto, Nanako, additional, Moriya-Ito, Keiko, additional, Komaki, Yuji, additional, Lee, Chia-Ying, additional, Okahara, Norio, additional, Guo, Xiaoli, additional, Harada, Chikako, additional, Kim, Euido, additional, Nakano, Tadashi, additional, Tsuneoka, Hiroshi, additional, Inoue, Takashi, additional, Sasaki, Erika, additional, Tokuno, Hironobu, additional, and Harada, Takayuki, additional

Published
2019
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46. Dock3-NMDA receptor interaction as a target for glaucoma therapy

Author

Kimura, Atsuko, Namekata, Kazuhiko, Guo, Xiaoli, Harada, Chikako, and Harada, Takayuki

Subjects
GluN2B, 6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología [CDU], Dock3, Glutamate neurotoxicity, Glaucoma, Neuroprotection
Abstract

y. Glaucoma is a neurodegenerative disease of the eye and it is one of the major causes of blindness. Glaucoma is usually associated with elevated intraocular pressure (IOP) and the current therapy focuses on reduction of IOP. However, neuroprotective strategies could also be beneficial for treatment of glaucoma because the pathology of the disease involves retinal ganglion cell (RGC) death and damage to the optic nerve. Dedicator of cytokinesis 3 (Dock3) is an atypical guanine exchange factor (GEF) that belongs to a family of Dock proteins, Dock1-11. Dock3 exerts neuroprotective effects on the retina and optic nerve, and studies revealed that some of the Dock3-mediated effects are GEF-independent. One of these mechanisms is that Dock3 directly binds to the GluN2B subunit of the Nmethyl-D-aspartate (NMDA) receptor. Upon stimulation by NMDA or optic nerve crush, overexpression of Dock3 promotes internalization and degradation of the NMDA receptor in the retina in vivo. It is suggested that this process is mediated by inhibition of Fyn, a Src family tyrosine kinase. Reduction in NMDA receptor expression results in decreased excitotoxic damage and oxidative stress, thereby promoting RGC survival. In this review, we discuss the therapeutic potential of neuroprotection for glaucoma and the effects of Dock3 on NMDA receptors. We also discuss apoptosis signalregulating kinase 1 (ASK1), a member of mitogenactivated protein kinase kinase kinase that is a key regulator of cellular responses to oxidative stress, as an innovative therapeutic target for glaucoma.

Published
2017

47. Targeting Oxidative Stress for Treatment of Glaucoma and Optic Neuritis

Author

Kimura, Atsuko, Namekata, Kazuhiko, Guo, Xiaoli, Noro, Takahiko, Harada, Chikako, and Harada, Takayuki

Subjects
genetic structures, Article Subject, sense organs, eye diseases
Abstract

Glaucoma is a neurodegenerative disease of the eye and it is one of the leading causes of blindness. Glaucoma is characterized by progressive degeneration of retinal ganglion cells (RGCs) and their axons, namely, the optic nerve, usually associated with elevated intraocular pressure (IOP). Current glaucoma therapies target reduction of IOP, but since RGC death is the cause of irreversible vision loss, neuroprotection may be an effective strategy for glaucoma treatment. One of the risk factors for glaucoma is increased oxidative stress, and drugs with antioxidative properties including valproic acid and spermidine, as well as inhibition of apoptosis signal-regulating kinase 1, an enzyme that is involved in oxidative stress, have been reported to prevent glaucomatous retinal degeneration in mouse models of glaucoma. Optic neuritis is a demyelinating inflammation of the optic nerve that presents with visual impairment and it is commonly associated with multiple sclerosis, a chronic demyelinating disease of the central nervous system. Although steroids are commonly used for treatment of optic neuritis, reduction of oxidative stress by approaches such as gene therapy is effective in ameliorating optic nerve demyelination in preclinical studies. In this review, we discuss oxidative stress as a therapeutic target for glaucoma and optic neuritis.

Published
2017
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