Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis

Pericytes are a population of cells that participate in normal vessel architecture and regulate permeability. Apelin, as the endogenous ligand of G protein-coupled receptor APJ, participates in a number of physiological and pathological processes. To date, the effect of apelin on pericyte is not cle...

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Main Authors: Li Chen, Yong Tao, Jing Feng, Yan Rong Jiang
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Journal of Ophthalmology
Online Access:http://dx.doi.org/10.1155/2015/186946
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author Li Chen
Yong Tao
Jing Feng
Yan Rong Jiang
author_facet Li Chen
Yong Tao
Jing Feng
Yan Rong Jiang
author_sort Li Chen
collection DOAJ
description Pericytes are a population of cells that participate in normal vessel architecture and regulate permeability. Apelin, as the endogenous ligand of G protein-coupled receptor APJ, participates in a number of physiological and pathological processes. To date, the effect of apelin on pericyte is not clear. Our study aimed to investigate the potential protection mechanisms of apelin, with regard to primary rat retinal pericytes under hypoxia. Immunofluorescence staining revealed that pericytes colocalized with APJ in the fibrovascular membranes dissected from proliferative diabetic retinopathy patients. In the in vitro studies, we first demonstrated that the expression of apelin/APJ was upregulated in pericytes under hypoxia, and apelin increased pericytes proliferation and migration. Moreover, knockdown of apelin in pericyte was achieved via lentivirus-mediated RNA interference. After the inhibition of apelin, pericytes proliferation was inhibited significantly in hypoxia culture condition. Furthermore, exogenous recombinant apelin effectively prevented hypoxia-induced apoptosis through downregulating active-caspase 3 expression and increasing the ratio of B cell lymphoma-2 (Bcl-2)/Bcl-2 associated X protein (Bax) in pericytes. These results suggest that apelin suppressed hypoxia-induced pericytes injury, which indicated that apelin could be a potential therapeutic target for retinal angiogenic diseases.
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spelling doaj-art-01269da5e4b349b6b94aa3e1ad3d10fa2025-02-03T05:58:44ZengWileyJournal of Ophthalmology2090-004X2090-00582015-01-01201510.1155/2015/186946186946Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced ApoptosisLi Chen0Yong Tao1Jing Feng2Yan Rong Jiang3Department of Ophthalmology, People’s Hospital, Peking University, 11 Xizhimen South Street, Xicheng District, Beijing 100044, ChinaDepartment of Ophthalmology, People’s Hospital, Peking University, 11 Xizhimen South Street, Xicheng District, Beijing 100044, ChinaDepartment of Ophthalmology, People’s Hospital, Peking University, 11 Xizhimen South Street, Xicheng District, Beijing 100044, ChinaDepartment of Ophthalmology, People’s Hospital, Peking University, 11 Xizhimen South Street, Xicheng District, Beijing 100044, ChinaPericytes are a population of cells that participate in normal vessel architecture and regulate permeability. Apelin, as the endogenous ligand of G protein-coupled receptor APJ, participates in a number of physiological and pathological processes. To date, the effect of apelin on pericyte is not clear. Our study aimed to investigate the potential protection mechanisms of apelin, with regard to primary rat retinal pericytes under hypoxia. Immunofluorescence staining revealed that pericytes colocalized with APJ in the fibrovascular membranes dissected from proliferative diabetic retinopathy patients. In the in vitro studies, we first demonstrated that the expression of apelin/APJ was upregulated in pericytes under hypoxia, and apelin increased pericytes proliferation and migration. Moreover, knockdown of apelin in pericyte was achieved via lentivirus-mediated RNA interference. After the inhibition of apelin, pericytes proliferation was inhibited significantly in hypoxia culture condition. Furthermore, exogenous recombinant apelin effectively prevented hypoxia-induced apoptosis through downregulating active-caspase 3 expression and increasing the ratio of B cell lymphoma-2 (Bcl-2)/Bcl-2 associated X protein (Bax) in pericytes. These results suggest that apelin suppressed hypoxia-induced pericytes injury, which indicated that apelin could be a potential therapeutic target for retinal angiogenic diseases.http://dx.doi.org/10.1155/2015/186946
spellingShingle Li Chen
Yong Tao
Jing Feng
Yan Rong Jiang
Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis
Journal of Ophthalmology
title Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis
title_full Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis
title_fullStr Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis
title_full_unstemmed Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis
title_short Apelin Protects Primary Rat Retinal Pericytes from Chemical Hypoxia-Induced Apoptosis
title_sort apelin protects primary rat retinal pericytes from chemical hypoxia induced apoptosis
url http://dx.doi.org/10.1155/2015/186946
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AT jingfeng apelinprotectsprimaryratretinalpericytesfromchemicalhypoxiainducedapoptosis
AT yanrongjiang apelinprotectsprimaryratretinalpericytesfromchemicalhypoxiainducedapoptosis