Chalcomoracin prevents vitreous-induced activation of AKT and migration of retinal pigment epithelial cells.

Abstract

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.

• Authors: Haote Han, Yanhui Yang, Bing Liu, Jingkui Tian, Lijun Dong, Hui Qi, Wei Zhu, Jiantao Wang, Hetian Lei
• Journal: Journal of cellular and molecular medicine (J Cell Mol Med) Vol. 25 Issue 19 Pg. 9102-9111 (10 2021) ISSN: 1582-4934 [Electronic] England
• PMID: 34432370 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.

Chemical References

• Benzofurans
• Tumor Suppressor Protein p53
• chalcomoracin
• Proto-Oncogene Proteins c-akt

Topics

• Animals
• Benzofurans (chemistry, pharmacology)
• Cell Line
• Cell Movement (drug effects)
• Cell Proliferation (drug effects)
• Cells, Cultured
• Epithelial Cells (drug effects, metabolism)
• Humans
• Proto-Oncogene Proteins c-akt (metabolism)
• Rabbits
• Retinal Pigment Epithelium (cytology, metabolism)
• Signal Transduction (drug effects)
• Tumor Suppressor Protein p53 (metabolism)
• Vitreous Body (metabolism)