Version 1
: Received: 18 April 2020 / Approved: 19 April 2020 / Online: 19 April 2020 (02:18:01 CEST)
How to cite:
Han, H.; Yang, Y.; Liu, B.; Tian, J.; Zhu, W.; Wang, J.; Lei, H. Chalcomoracin Prevents Vitreous-Induced Activation of AKT and Migration of Retinal Pigment Epithelial Cells. Preprints2020, 2020040312 (doi: 10.20944/preprints202004.0312.v1).
Han, H.; Yang, Y.; Liu, B.; Tian, J.; Zhu, W.; Wang, J.; Lei, H. Chalcomoracin Prevents Vitreous-Induced Activation of AKT and Migration of Retinal Pigment Epithelial Cells. Preprints 2020, 2020040312 (doi: 10.20944/preprints202004.0312.v1).
Cite as:
Han, H.; Yang, Y.; Liu, B.; Tian, J.; Zhu, W.; Wang, J.; Lei, H. Chalcomoracin Prevents Vitreous-Induced Activation of AKT and Migration of Retinal Pigment Epithelial Cells. Preprints2020, 2020040312 (doi: 10.20944/preprints202004.0312.v1).
Han, H.; Yang, Y.; Liu, B.; Tian, J.; Zhu, W.; Wang, J.; Lei, H. Chalcomoracin Prevents Vitreous-Induced Activation of AKT and Migration of Retinal Pigment Epithelial Cells. Preprints 2020, 2020040312 (doi: 10.20944/preprints202004.0312.v1).
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 if Chalocomoracin (CMR), a novel purified compound from fungus-infected mulberry leaves, is able to inhibit vitreous-induced signaling events and cellular responses intrinsic to PVR. Our studies have revealed that the CMR IC50 for ARPE-19 cells is 35.5 μM at 72 hours, and that 5 μM 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.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
