Role of Nogo receptor in glucocorticoids-induced apoptosis of retinal ganglion cell
AIM: To explore the effects and underlying mechanisms of glucocorticoid in the apoptosis of retinal ganglion cell(RGC).<p>METHODS: RGC were cultured in 4 groups for 3d: control group, glucocorticoid group(with 0.1μmol/L cortisone), glucocorticoid-siNgR group \〖with 0.1μmol/L cortisone+Nogo rec...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
Press of International Journal of Ophthalmology (IJO PRESS)
2015-06-01
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| Series: | Guoji Yanke Zazhi |
| Subjects: | |
| Online Access: | http://ies.ijo.cn/cn_publish/2015/6/201506009.pdf |
| Summary: | AIM: To explore the effects and underlying mechanisms of glucocorticoid in the apoptosis of retinal ganglion cell(RGC).<p>METHODS: RGC were cultured in 4 groups for 3d: control group, glucocorticoid group(with 0.1μmol/L cortisone), glucocorticoid-siNgR group \〖with 0.1μmol/L cortisone+Nogo receptor(NgR)antisense nucleotide\〗, glucocorticoid-scRNA group(with 0.1μmol/L cortisone + scrambled nucleotide). The cell viability was detected by thiazolyl blue tetrazolium bromide(MTT), the morphological features were observed with inverted microscope, apoptosis of RGC was measured with Hoechst 33342 staining, and expression of NgR was revealed by Western blot. <p>RESULTS: Cell viability in control, glucocorticoid, glucocorticoid-scRNA and glucocorticoid-siNgR groups were(100.0±0.0)%,(76.3±6.8)%,(79.4±9.0)% and(96.7±9.8)% respectively. Decreased cell viability, reduced cell number, and increased expression of NgR were atrophic cell body detected in glucocorticoid and glucocorticoid-scRNA groups(<i>P</i><0.01), not in glucocorticoid-siNgR group(<i>P</i>>0.05), compared with control group. RGC was showed light blue by Hoechst 33 342 staining in control and glucocorticoid-siNgR groups, and exhibiting bright blued apoptotic RGC in glucocorticoid and glucocorticoid-scRNA groups.<p>CONCLUSION: Up-regulation of NgR contributes to glucocorticoids-induced apoptosis of RGC. |
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| ISSN: | 1672-5123 1672-5123 |