Open AccessChalcomoracin prevents vitreous‐induced activation of AKT and migration of retinal pigment epithelial cells
Author(s) -
Han Haote,
Yang Yanhui,
Liu Bing,
Tian Jingkui,
Dong Lijun,
Qi Hui,
Zhu Wei,
Wang Jiantao,
Lei Hetian
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16590
Subject(s) - proliferative vitreoretinopathy , retinal , protein kinase b , microbiology and biotechnology , pathogenesis , chemistry , retinal pigment epithelium , pigment , retinal detachment , macular degeneration , signal transduction , cancer research , medicine , ophthalmology , biology , pathology , biochemistry , organic chemistry
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.