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망막신경절세포에서 헴산화효소 발현에 의한 Betaxolol의 세포보호효과
차재봉(Jae Bong Cha),권민영(Min Young Kwon),정수월(Su Wol Chung),우제문(Je Moon Woo) 대한안과학회 2016 대한안과학회지 Vol.57 No.1
Purpose: To evaluate the neuroprotective effects of betaxolol (betaxolol hydrochloride) under hypoxic conditions using retinal ganglion cells (RGC-5) and determine whether heme oxygenase-1 (HO-1) expression exerts cytoprotective effects. Methods: In this study, cultured RGC-5 cells were incubated with different concentrations of betaxolol hydrochloride (0.1 μM, 1μM or 5 μM) and with 10 μM zinc protoporphyrin (ZnPP), in a hypoxia incubator (1% O2, 5% CO2, 94% N2) for 48 hours and the cell viability of each group was determined. Additionally, cell viability was measured after RGC-5 cells were incubated with 5 μM of brinzolamide (Azopt??), brimonidine tartrate (Alphagan??) or travoprost (Travatan??). RGC-5 cells were divided into three groups and incubated under three different conditions, normoxia group (20% O2, 5% CO2), hypoxia group (1% O2, 5% CO2) and the group with 5 μM of Betoptic S?? treated under hypoxic conditions (hypoxia, Betoptic S??). After incubation for 4, 8, 12 and 24 hours, HO-1 expression was analyzed using Western blotting. Results: Cell viability significantly increased in RGC-5 cells treated with Betoptic S?? compared with other antiglaucoma agents. Increased levels of HO-1 expression indicate its relevance in cell viability. Furthermore, increased RGC-5 cell viability by Betoptic S?? was significantly reduced in the HO-1 inhibitor ZnPP-treated group. Conclusions: We reaffirmed the known cytoprotective effects of Betoptic S?? and the results suggests that HO-1 expression exerts cytoprotective effects against hypoxia.
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황나래,권민영,차재봉,정수월,우제문 대한안과학회 2016 Korean Journal of Ophthalmology Vol.30 No.6
Purpose: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmicreticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluatedin the human retinal pigment epithelial cell line, ARPE-19. Methods: PTX3 production in ARPE-19 cells was analyzed in the absence or presence of tunicamycin treatmentby enzyme-linked immunosorbent assay. PTX3 protein and mRNA levels were estimated using western blotanalysis and real-time reverse transcription-polymerase chain reaction, respectively. Protein and mRNA levelsof CCAAT-enhancer-binding protein homologous protein (CHOP) and ARPE-19 cell viability were measuredin the presence of tunicamycin-induced ER stress in control or PTX3 small hairpin RNA (shRNA)-transfectedARPE-19 cells. Results: The protein and mRNA levels of PTX3 were found to be significantly increased by tunicamycin treatment. PTX3 production was significantly decreased in inositol-requiring enzyme 1α shRNA-transfected ARPE-19 cells compared to control shRNA-transfected cells. Furthermore, pretreatment with the NF-kB inhibitorabolished tunicamycin-induced PTX3 production. Decreased cell viability and prolonged protein and mRNAexpression of CHOP were observed under tunicamycin-induced ER stress in PTX3 shRNA transfected ARPE-19 cells. Conclusions: These results suggest that PTX3 production increased in the presence of tunicamycin-inducedER stress. Therefore, PTX3 could be an important protector of ER stress-induced cell death in human retinalpigment epithelial cells. Inositol-requiring enzyme 1α and the NF-kB signaling pathway may serve as potentialtargets for regulation of PTX3 expression in the retina. Therefore, their role in PTX3 expression needs to befurther investigated.
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