Abstract |
OBJECTIVE: To explore the molecular mechanism of diabetic internal environment in regulating the endoplasmic reticulum stress of the retinal ganglion cells (RGCs). METHODS: RESULTS:
Glaucoma promotes the apoptosis of RGCs. The protein expression values of RTN4IP1, PERK and XBP1 in DM mouse models with glaucoma were much higher compared to only DM mouse models. Further injection of endoplasmic reticulum stress inhibitor 4-PBA decreased the expression values. The relative mRNA levels of CHOP, Cysteine aspartic acid specific protease12 (Caspase12) and BCL2-associated X protein (Bax) in DM + glaucoma were significantly higher compared to those in DM group. Further injection of endoplasmic reticulum stress inhibitor 4-PBA decreased the mRNA levels. CONCLUSION: Endoplasmic reticulum stress (ERS) is the underlying cause of glaucoma, which could promote the apoptosis of RGCs in diabetic mice.
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Authors | Jinzi Zhou, Fenghua Chen, Aimin Yan, Jian Jiang, Xiaobo Xia |
Journal | Transplant immunology
(Transpl Immunol)
Vol. 73
Pg. 101636
(08 2022)
ISSN: 1878-5492 [Electronic] Netherlands |
PMID | 35659921
(Publication Type: Journal Article)
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Copyright | Copyright © 2022 Elsevier B.V. All rights reserved. |
Chemical References |
- Carrier Proteins
- Mitochondrial Proteins
- RNA, Messenger
- bcl-2-Associated X Protein
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Topics |
- Animals
- Apoptosis
- Carrier Proteins
(metabolism)
- Diabetes Mellitus, Experimental
(metabolism)
- Diabetes Mellitus, Type 2
(metabolism)
- Endoplasmic Reticulum Stress
- Glaucoma
(metabolism)
- Hyperglycemia
- Mice
- Mice, Inbred C57BL
- Mitochondrial Proteins
- Neurodegenerative Diseases
(metabolism)
- RNA, Messenger
- Retinal Ganglion Cells
(metabolism)
- bcl-2-Associated X Protein
(metabolism)
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