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28 results on '"Higashijima, Fumiaki"'

7. HIF-1α-dependent upregulation of angiogenic factors by mechanical stimulation in retinal pigment epithelial cells

Author

Ashimori, Atsushige, primary, Higashijima, Fumiaki, additional, Ogata, Tadahiko, additional, Sakuma, Ayano, additional, Hamada, Waka, additional, Sunada, Junki, additional, Aoki, Ren, additional, Mikuni, Masanori, additional, Hayashi, Ken'ichiro, additional, Wakuta, Makiko, additional, Yoshimoto, Takuya, additional, Minamoto, Akira, additional, Ko, Ji-Ae, additional, and Kimura, Kazuhiro, additional

Published
2024
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8. Characterization of the visually impaired patients with diabetes mellitus in Japan

Author

Sugihara, Yuka, primary, Takamura, Yoshihiro, additional, Yamada, Yutaka, additional, Morioka, Masakazu, additional, Gozawa, Makoto, additional, Kato, Kumiko, additional, Hirano, Takao, additional, Murao, Fumiko, additional, Shimizu, Miho, additional, Kusuhara, Sentaro, additional, Murakami, Tomoya, additional, Takenaka, Yuki, additional, Okabe, Naoko, additional, Jujo, Tatsuya, additional, Terasaki, Hiroto, additional, Nagasato, Daisuke, additional, Dong, Zhenyu, additional, Yoshida, Shigeo, additional, Ogura, Shuntaro, additional, Yasuda, Kanako, additional, Ishigooka, Gaku, additional, Sawada, Osamu, additional, Higashijima, Fumiaki, additional, and Inatani, Masaru, additional

Published
2024
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12. SARS-CoV-2 infection status in corneal preservation solution and COVID-19 prevalence after corneal transplantation

Author

Wasai, Yuki, primary, Yamada, Naoyuki, additional, Ariyoshi, Nobuaki, additional, Haraguchi, Aiko, additional, Funatsu, Masahiko, additional, Mikuni, Masanori, additional, Nakamura, Riku, additional, Sakuma, Ayano, additional, Higashijima, Fumiaki, additional, Iwamoto, Nanako, additional, Teranishi, Shinichiro, additional, Nishioka, Mitsuaki, additional, Yamasaki, Takahiro, additional, and Kimura, Kazuhiro, additional

Published
2023
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14. Exacerbation of Diabetic Retinopathy following Hypoxia-Inducible Factor-Prolyl Hydroxylase Inhibitor Administration: A Case Report.

Author

Ariyoshi, Nobuaki, Higashijima, Fumiaki, Wakuta, Makiko, Ogata, Tadahiko, Ohta, Manami, and Kimura, Kazuhiro

Subjects
*DIABETIC nephropathies, *DIABETIC retinopathy, *VASCULAR endothelial growth factors, *OPTICAL coherence tomography, *FLUORESCENCE angiography, *RETINAL diseases, *DISEASE exacerbation
Abstract

Introduction: Hypoxia-inducible factor-prolyl hydroxylase (HIF-PH) inhibitors, used in the treatment of renal anemia, hold the potential to increase the production of vascular endothelial growth factors. Therefore, HIF-PH inhibitors may exacerbate retinal hemorrhage in diseases such as diabetic retinopathy. Here, we present a case involving the administration of an HIF-PH inhibitor, resulting in the exacerbation of retinal hemorrhage in a patient with diabetic retinopathy. Case Presentation: A 32-year-old man with diabetes mellitus and renal anemia caused by diabetic nephropathy was referred to our department for ophthalmic examination, revealing diabetic retinopathy with scattered retinal hemorrhages, exudates, and diabetic maculopathy in both eyes. Darbepoetin alfa was initially administered and switched to the HIF-PH inhibitor roxadustat on day 74. By day 88, fresh retinal hemorrhage was observed in the right eye. On day 132, the retinal hemorrhage had further worsened, with new preretinal hemorrhage in both eyes. Roxadustat was discontinued, replaced with darbepoetin alfa, resulting in retinal hemorrhage improvement by day 181 (49 days post-roxadustat cessation). On day 201, fundus hemorrhage further improved, optical coherence tomography showed no macular edema or subretinal fluid, and the retina was thinning. Fluorescein angiography showed neovascular vessels, active fluorescein leakage, and extensive avascular areas in both eyes, prompting pan-retinal photocoagulation. Visual acuity remained stable throughout treatment. Conclusion: Patients with advanced diabetic retinopathy taking HIF-PH inhibitors should be aware of retinal hemorrhage exacerbations. If observed, the treatment plan, including discontinuation of the HIF-PH inhibitor or switching to another agent, should be discussed with a diabetologist, nephrologist, and ophthalmologist. [ABSTRACT FROM AUTHOR]

Published
2024
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15. Early manifestations and differential gene expression associated with photoreceptor degeneration in Prom1-deficient retina

Author

Kobayashi, Yuka, Watanabe, Shizuka, Ong, Agnes Lee Chen, Shirai, Manabu, Yamashiro, Chiemi, Ogata, Tadahiko, Higashijima, Fumiaki, Yoshimoto, Takuya, Hayano, Takahide, Asai, Yoshiyuki, Sasai, Noriaki, Kimura, Kazuhiro, Kobayashi, Yuka, Watanabe, Shizuka, Ong, Agnes Lee Chen, Shirai, Manabu, Yamashiro, Chiemi, Ogata, Tadahiko, Higashijima, Fumiaki, Yoshimoto, Takuya, Hayano, Takahide, Asai, Yoshiyuki, Sasai, Noriaki, and Kimura, Kazuhiro

Abstract

Retinitis pigmentosa (RP) and macular dystrophy (MD) are characterized by gradual photoreceptor death in the retina and are often associated with genetic mutations, including those in the prominin-1 (Prom1) gene. Prom1-knockout (KO) mice recapitulate key features of these diseases including light-dependent retinal degeneration and constriction of retinal blood vessels. The mechanisms underlying such degeneration have remained unclear, however. We here analysed early events associated with retinal degeneration in Prom1-KO mice. We found that photoreceptor cell death and glial cell activation occur between 2 and 3 weeks after birth. Whereas gene expression was not affected at 2 weeks, the expression of several genes was altered at 3 weeks in the Prom1-KO retina, with the expression of that for endothelin-2 (Edn2) being markedly upregulated. Expression of Edn2 was also induced by light stimulation in Prom1-KO mice reared in the dark. Treatment with endothelin receptor antagonists attenuated photoreceptor cell death, gliosis and retinal vessel stenosis in Prom1-KO mice. Our findings thus reveal early manifestations of retinal degeneration in a model of RP/MD and suggest potential therapeutic agents for these diseases.This article has an associated First Person interview with the first author of the paper.

Published
2023

17. Role of CRP2-MRTF interaction in functions of myofibroblasts

Author

Hayashi, Ken’ichiro, primary, Horoiwa, Shinri, additional, Mori, Kotaro, additional, Miyata, Hiroshi, additional, Labios, Reuben Jacob, additional, Morita, Tsuyoshi, additional, Kobayashi, Yuka, additional, Yamashiro, Chiemi, additional, Higashijima, Fumiaki, additional, Yoshimoto, Takuya, additional, Kimura, Kazuhiro, additional, and Nakagawa, Yoshiaki, additional

Published
2023
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20. Prominin‐1 deletion results in spermatogenic impairment, sperm morphological defects, and infertility in mice.

Author

Matsukuma, Haruka, Kobayashi, Yuka, Oka, Shintaro, Higashijima, Fumiaki, Kimura, Kazuhiro, Yoshihara, Erika, Sasai, Noriaki, and Shiraishi, Koji

Subjects
INFERTILITY, EPITHELIAL cells, SPERMATOGENESIS, SPERM motility, MICE, MALE infertility
Abstract

Purpose: Spermatogenesis is a complex process orchestrated by several essential genes. Prominin‐1 (Prom1/PROM1) is a gene that is expressed in the testis but with a poorly understood role in spermatogenesis. Methods: We used Prom1 knockout (Prom1 KO) mice to assess the role of Prom1 in spermatogenesis. To this end, we performed immunohistochemistry, immunofluorescence, western blotting, β‐galactosidase staining, and apoptosis assay. Additionally, we analyzed the morphology of sperm and assessed litter sizes. Results: We observed that PROM1 is localized to the dividing spermatocytes in seminiferous epithelial cells, sperm, and columnar epithelium in the epididymis. In the Prom1 KO testis, an aberrant increase in apoptotic cells and a decrease in proliferating seminiferous epithelial cells were observed. Cellular FLICE‐like inhibitory protein (c‐FLIP) and extracellular signal‐regulated kinase 1/2 (ERK1/2) expression were also significantly decreased in Prom1 KO testis. In addition, a significantly increased number of epididymal spermatozoa with abnormal morphology and less motility was found in Prom1 KO mice. Conclusions: PROM1 maintains spermatogenic cell proliferation and survival via c‐FLIP expression in the testis. It is also involved in sperm motility and fertilization potential. The mechanism underlying the effect of Prom1 on sperm morphology and motility remains to be identified. [ABSTRACT FROM AUTHOR]

Published
2023
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21. Early manifestations and differential gene expression associated with photoreceptor degeneration in Prom1-deficient retina

Author

Kobayashi, Yuka, primary, Watanabe, Shizuka, additional, Ong, Agnes Lee Chen, additional, Shirai, Manabu, additional, Yamashiro, Chiemi, additional, Ogata, Tadahiko, additional, Higashijima, Fumiaki, additional, Yoshimoto, Takuya, additional, Hayano, Takahide, additional, Asai, Yoshiyuki, additional, Sasai, Noriaki, additional, and Kimura, Kazuhiro, additional

Published
2021
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24. Early manifestations and differential gene expression associated with photoreceptor degeneration in Prom1-deficient retina

Author

Kobayashi, Yuka, Watanabe, Shizuka, Ong, Agnes Lee Chen, Shirai, Manabu, Yamashiro, Chiemi, Ogata, Tadahiko, Higashijima, Fumiaki, Yoshimoto, Takuya, Hayano, Takahide, Asai, Yoshiyuki, Sasai, Noriaki, Kimura, Kazuhiro, Kobayashi, Yuka, Watanabe, Shizuka, Ong, Agnes Lee Chen, Shirai, Manabu, Yamashiro, Chiemi, Ogata, Tadahiko, Higashijima, Fumiaki, Yoshimoto, Takuya, Hayano, Takahide, Asai, Yoshiyuki, Sasai, Noriaki, and Kimura, Kazuhiro

Abstract

Retinitis pigmentosa (RP) and macular dystrophy (MD) are characterized by gradual photoreceptor death in the retina and are often associated with genetic mutations, including those in the prominin-1 (Prom1) gene. Prom1-knockout (KO) mice recapitulate key features of these diseases including light-dependent retinal degeneration and constriction of retinal blood vessels. The mechanisms underlying such degeneration have remained unclear, however. We here analysed early events associated with retinal degeneration in Prom1-KO mice. We found that photoreceptor cell death and glial cell activation occur between 2 and 3 weeks after birth. Whereas gene expression was not affected at 2 weeks, the expression of several genes was altered at 3 weeks in the Prom1-KO retina, with the expression of that for endothelin-2 (Edn2) being markedly upregulated. Expression of Edn2 was also induced by light stimulation in Prom1-KO mice reared in the dark. Treatment with endothelin receptor antagonists attenuated photoreceptor cell death, gliosis and retinal vessel stenosis in Prom1-KO mice. Our findings thus reveal early manifestations of retinal degeneration in a model of RP/MD and suggest potential therapeutic agents for these diseases. This article has an associated First Person interview with the first author of the paper., identifier:1754-8403

Published
2021

25. Light-dependent induction of Edn2 expression and attenuation of retinal pathology by endothelin receptor antagonists in Prominin-1- deficient mice

Author

Kobayashi Yuka, Higashijima Fumiaki, Sasai Noriaki, Watanabe Shizuka, Shirai Manabu, Kimura Kazuhiro, Ogata Tadahiko, Hayano Takahide, Yoshimoto Takuya, Asai Yoshiyuki, and Yamashiro Chiemi

Subjects
Retinal degeneration, Pathology, medicine.medical_specialty, Retina, business.industry, Retinal, medicine.disease, Photoreceptor cell, chemistry.chemical_compound, medicine.anatomical_structure, chemistry, Gliosis, Retinitis pigmentosa, medicine, medicine.symptom, Endothelin receptor, business, Cell activation
Abstract

Retinitis pigmentosa (RP) and macular dystrophy (MD) are prevalent retinal degenerative diseases associated with gradual photoreceptor death. These diseases are often caused by genetic mutations that result in degeneration of the retina postnatally after it has fully developed. The Prominin-1 gene (Prom1) is a causative gene for RP and MD, and Prom1- knockout (KO) mice recapitulate key features of these diseases including light-dependent retinal degeneration and stenosis of retinal blood vessels. The mechanisms underlying progression of such degeneration have remained unknown, however. We here analysed early events associated with retinal degeneration in Prom1-KO mice. We found that photoreceptor cell death and glial cell activation occur between 2 and 3 weeks after birth. High-throughput analysis revealed that expression of the endothelin-2 gene (Edn2) was markedly up-regulated in the Prom1-deficient retina during this period. Expression of Edn2 was also induced by light stimulation in Prom1-KO mice that had been reared in the dark. Finally, treatment with endothelin receptor antagonists attenuated photoreceptor cell death, gliosis, and retinal vessel stenosis in Prom1-KO mice. Our findings suggest that inhibitors of endothelin signalling may delay the progression of RP and MD and therefore warrant further study as potential therapeutic agents for these diseases.

Published
2020
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26. Light-dependent induction of Edn2 expression and attenuation of retinal pathology by endothelin receptor antagonists in Prominin-1- deficient mice

Author

Kobayashi, Yuka, primary, Watanabe, Shizuka, additional, Shirai, Manabu, additional, Yamashiro, Chiemi, additional, Ogata, Tadahiko, additional, Higashijima, Fumiaki, additional, Yoshimoto, Takuya, additional, Hayano, Takahide, additional, Asai, Yoshiyuki, additional, Sasai, Noriaki, additional, and Kimura, Kazuhiro, additional

Published
2020
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27. Influence of extended depth of focus intraocular lenses on visual field sensitivity

Author

Takahashi, Makiko, primary, Yamashiro, Chiemi, additional, Yoshimoto, Takuya, additional, Kobayashi, Yuka, additional, Higashijima, Fumiaki, additional, Kobayashi, Masaaki, additional, Hatano, Makoto, additional, Ohta, Manami, additional, Nagai, Tomohiko, additional, Teranishi, Shinichiro, additional, Suzuki, Katsuyoshi, additional, Takabatake, Ryu, additional, and Kimura, Kazuhiro, additional

Published
2020
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