PMC:5118426 / 32469-33602 JSONTXT

{"project":"MyTest","denotations":[{"id":"27920719-17213800-31054381","span":{"begin":194,"end":198},"obj":"17213800"},{"id":"27920719-26469749-31054382","span":{"begin":467,"end":471},"obj":"26469749"},{"id":"27920719-25804419-31054383","span":{"begin":932,"end":936},"obj":"25804419"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"TUDCA ameliorated cell death and loss of photoreceptor function after exposure to high levels of light (10,000 lux) that can induce retinal degeneration in albino Balb/C mice (Boatright et al., 2006). TUDCA pre-treatment of ex vivo perfused whole mount feline retinas repeatedly exposed to light stimulation and dark adaptations over 5 h resulted in greater receptive field size, decreased irradiance threshold, and maintenance of the contrast threshold (Xia et al., 2015). Retinal dystrophy can be caused by defects in the phagocytosis by retinal pigment epithelium cells of the photoreceptor outer segments that are shed, a continuous and extremely active process involving thousands of shed membranous disks each day. TUDCA was found to increase phagocytic activity and inhibit hydrogen peroxide induced impairment of phagocytosis by both cultured ARPE-19 cells and primary human retinal pigment epithelium cells (Murase et al., 2015). The phosphorylation of MerTK was significantly increased by TUDCA in a concentration-dependent manner but did not affect expression of the ER stress marker glucose regulated protein-78 (GRP-78)."}

{"project":"2_test","denotations":[{"id":"27920719-17213800-31054381","span":{"begin":194,"end":198},"obj":"17213800"},{"id":"27920719-26469749-31054382","span":{"begin":467,"end":471},"obj":"26469749"},{"id":"27920719-25804419-31054383","span":{"begin":932,"end":936},"obj":"25804419"}],"text":"TUDCA ameliorated cell death and loss of photoreceptor function after exposure to high levels of light (10,000 lux) that can induce retinal degeneration in albino Balb/C mice (Boatright et al., 2006). TUDCA pre-treatment of ex vivo perfused whole mount feline retinas repeatedly exposed to light stimulation and dark adaptations over 5 h resulted in greater receptive field size, decreased irradiance threshold, and maintenance of the contrast threshold (Xia et al., 2015). Retinal dystrophy can be caused by defects in the phagocytosis by retinal pigment epithelium cells of the photoreceptor outer segments that are shed, a continuous and extremely active process involving thousands of shed membranous disks each day. TUDCA was found to increase phagocytic activity and inhibit hydrogen peroxide induced impairment of phagocytosis by both cultured ARPE-19 cells and primary human retinal pigment epithelium cells (Murase et al., 2015). The phosphorylation of MerTK was significantly increased by TUDCA in a concentration-dependent manner but did not affect expression of the ER stress marker glucose regulated protein-78 (GRP-78)."}