Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway
Purpose. Recent research has provided novel insight into the function of fibromodulin (FMOD) in wound healing and angiogenesis. The role of FMOD in initiation of proliferative vitreoretinopathy (PVR) has not been studied. This study investigated the effect of FMOD on human retinal pigment epithelial...
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Wiley
2018-01-01
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Series: | Journal of Ophthalmology |
Online Access: | http://dx.doi.org/10.1155/2018/5708537 |
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author | He Hu Shanshan Li Jianqiao Li Chao Huang Fang Zhou Li Zhao Wenzhen Yu Xiao Qin |
author_facet | He Hu Shanshan Li Jianqiao Li Chao Huang Fang Zhou Li Zhao Wenzhen Yu Xiao Qin |
author_sort | He Hu |
collection | DOAJ |
description | Purpose. Recent research has provided novel insight into the function of fibromodulin (FMOD) in wound healing and angiogenesis. The role of FMOD in initiation of proliferative vitreoretinopathy (PVR) has not been studied. This study investigated the effect of FMOD on human retinal pigment epithelial (RPE) cell, which plays an essential role in the progression of PVR, and the possible mechanisms. Methods. Small interfering (si) RNA-based gene transfer technology was used to decrease FMOD expression and to study its effects on RPEs in vitro. Cell Counting Kit-8 assays, transwells, and flow cytometry analysis were used to measure cell proliferation, migration, cell cycle, and apoptosis. Western blot was used to measure expression of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), extracellular signal-related kinase 1/2 (ERK1/2), and phosphoinositide 3 kinase (PI3K/AKT). Results. After transfection of RPEs with a FMOD-specific siRNA, cell proliferation and migration were inhibited to the percentage of 65% ± 5% and 39% ± 10%, respectively, compared to the control group. Depletion of FMOD induced cell cycle arrest and apoptosis in RPE cells. Downregulation of VEGF, VEGFR2, and phosphorylated AKT (p-AKT) were detected in transfected RPEs. Conclusion. Depletion of FMOD selectively downregulated the expression of VEGF and VEGFR2 and inhibited the signaling pathway of AKT phosphorylation, which consequently inhibited the proliferation and migration of RPE Cell. |
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id | doaj-art-938e9b99e9904bd8a7e5d48d7f4a1c27 |
institution | Kabale University |
issn | 2090-004X 2090-0058 |
language | English |
publishDate | 2018-01-01 |
publisher | Wiley |
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series | Journal of Ophthalmology |
spelling | doaj-art-938e9b99e9904bd8a7e5d48d7f4a1c272025-02-03T01:21:08ZengWileyJournal of Ophthalmology2090-004X2090-00582018-01-01201810.1155/2018/57085375708537Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT PathwayHe Hu0Shanshan Li1Jianqiao Li2Chao Huang3Fang Zhou4Li Zhao5Wenzhen Yu6Xiao Qin7Medical College, Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia, ChinaDepartment of Ophthalmology, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Ophthalmology, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Ophthalmology, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Ophthalmology, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Blood Transfusion, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Ophthalmology, Peking University People’s Hospital, Key Laboratory of Vision Loss and Restoration, Ministry of Education, Beijing Key Laboratory of Diagnosis and Therapy of Retinal and Choroid Diseases, Beijing, ChinaDepartment of Ophthalmology, Affiliated Hospital of Inner Mongolia University for the Nationalities, Tongliao, Inner Mongolia, ChinaPurpose. Recent research has provided novel insight into the function of fibromodulin (FMOD) in wound healing and angiogenesis. The role of FMOD in initiation of proliferative vitreoretinopathy (PVR) has not been studied. This study investigated the effect of FMOD on human retinal pigment epithelial (RPE) cell, which plays an essential role in the progression of PVR, and the possible mechanisms. Methods. Small interfering (si) RNA-based gene transfer technology was used to decrease FMOD expression and to study its effects on RPEs in vitro. Cell Counting Kit-8 assays, transwells, and flow cytometry analysis were used to measure cell proliferation, migration, cell cycle, and apoptosis. Western blot was used to measure expression of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), extracellular signal-related kinase 1/2 (ERK1/2), and phosphoinositide 3 kinase (PI3K/AKT). Results. After transfection of RPEs with a FMOD-specific siRNA, cell proliferation and migration were inhibited to the percentage of 65% ± 5% and 39% ± 10%, respectively, compared to the control group. Depletion of FMOD induced cell cycle arrest and apoptosis in RPE cells. Downregulation of VEGF, VEGFR2, and phosphorylated AKT (p-AKT) were detected in transfected RPEs. Conclusion. Depletion of FMOD selectively downregulated the expression of VEGF and VEGFR2 and inhibited the signaling pathway of AKT phosphorylation, which consequently inhibited the proliferation and migration of RPE Cell.http://dx.doi.org/10.1155/2018/5708537 |
spellingShingle | He Hu Shanshan Li Jianqiao Li Chao Huang Fang Zhou Li Zhao Wenzhen Yu Xiao Qin Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway Journal of Ophthalmology |
title | Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway |
title_full | Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway |
title_fullStr | Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway |
title_full_unstemmed | Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway |
title_short | Knockdown of Fibromodulin Inhibits Proliferation and Migration of RPE Cell via the VEGFR2-AKT Pathway |
title_sort | knockdown of fibromodulin inhibits proliferation and migration of rpe cell via the vegfr2 akt pathway |
url | http://dx.doi.org/10.1155/2018/5708537 |
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