Chalcomoracin prevents vitreous-induced activation of AKT and migration of retinal pigment epithelial cells
- J Cell Mol Med. 2021 Oct;25(19):9102-9111. doi: 10.1111/jcmm.16590.
- 1. Institute of Cancer and Basic Medicine, Chinese Academy of Sciences, Zhejiang Cancer Hospital, Cancer Hospital of the University of Chinese Academy of Sciences, Hangzhou, China.
- 2. College of Biomedical Engineering & Instrument Science, Zhejiang University, Hangzhou, China.
- 3. Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, USA.
- 4. Department of Ophthalmology, Harvard Medical School, Boston, MA, USA.
- 5. School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
- 6. Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
- 7. Shenzhen Eye Hospital, Shenzhen Eye Institute, Jinan University, Shenzhen, China.
Retinal pigment epithelial (RPE) cells are the major cell type in the epi- or sub-retinal membranes in the pathogenesis of proliferative vitreoretinopathy (PVR), which is a blinding fibrotic eye disease and still short of effective medicine. The purpose of this study is to demonstrate whether Chalocomoracin (CMR), a novel purified compound from fungus-infected mulberry leaves, is able to inhibit vitreous-induced signalling events and cellular responses intrinsic to PVR. Our studies have revealed that the CMR IC50 for ARPE-19 cells is 35.5 μmol/L at 72 hours, and that 5 μmol/L CMR inhibits vitreous-induced Akt activation and p53 suppression; in addition, we have discovered that this chemical effectively blocks vitreous-stimulated proliferation, migration and contraction of ARPE-19 cells, suggesting that CMR is a promising PVR prophylactic.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: ERK; JNK; p38 MAPK; PERK; mTOR; Akt; MDM-2/p53; PINK1/Parkin; Apoptosis; Reactive Oxygen Species (ROS); Paraptosis; Mitophagy; Autophagy; Bacterial; Glycosidase