Bone Marrow-Derived Cells in Neovascular Age-Related Macular Degeneration: Contribution and Potential Application

Hou, Huiyuan; Liu, Hongliang; Wang, Yusheng

doi:10.1159/000313983

Cited by 8 publications

(5 citation statements)

References 47 publications

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“…A crucial pathological aspect of age-related macular degeneration is choroidal neovascularization (CNV), which involves angiogenesis and vasculogenesis and causes severe visual impairments due to the leakage of immature blood vessels and subsequent fibrosis. Studies in recent decades have made considerable progress in exploring the pathogenesis of CNV and the development of new therapeutic approaches [2]. However, the exact mechanism of CNV has not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

CXCR7/CXCR4/CXCL12 Axis Regulates the Proliferation, Migration, Survival and Tube Formation of Choroid-Retinal Endothelial Cells

2013

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Background/Aims: Stromal cell-derived factor-1 (SDF-1) has been shown to mediate a broad range of biological processes via CXCR4, once regarded as its only receptor. CXCR7 is a recently identified receptor for SDF-1. This study aimed to investigate whether the CXCR7/CXCR4/SDF-1 axis is involved in choroidal neovascularization (CNV) formation in an in vitro hypoxic model. Methods: CXCR7 siRNA and/or CXCR4 siRNA was transfected into a hypoxic model of the choroid-retinal endothelial RF/6A cell line. CCK-8 analysis, transwell migration analysis, annexin V-FITC and propidium iodide staining, and Matrigel tube formation analysis were performed to investigate the role of CXCR4 and CXCR7 in SDF-1-induced proliferation, migration, survival and tube formation of RF/6A cells. Results: CXCR4, but not CXCR7, mediates SDF-1-induced RF/6A cell migration and proliferation under hypoxic conditions, whereas CXCR7 was exclusively involved in RF/6A cell survival. In addition, CXCR7 and CXCR4 acted together to regulate RF/6A cell tube formation. Conclusion: The CXCR7/CXCR4/SDF-1 axis plays an important role in the formation of CNV, and may become a novel target for the treatment of CNV-associated diseases.

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Section: Introductionmentioning

confidence: 99%

CXCR7/CXCR4/CXCL12 Axis Regulates the Proliferation, Migration, Survival and Tube Formation of Choroid-Retinal Endothelial Cells

2013

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“…Recent studies suggest an important role for endothelial progenitor cells (EPCs), hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs) in ocular neovascularization [ 4 ]. These stem cells have been shown to differentiate into different several cell types, including vascular components (vascular ECs, vascular smooth muscle cells (VSMCs), and pericytes) and extravascular cells (myofibroblasts, inflammatory cells, retinal pigment epithelial (RPE) cells and glial cells) [ 1 ]. In addition to stem cells, bone marrow (BM)-derived macrophages are key modulators of the severity of ocular neovascularization.…”

Section: Bone Marrow-derived Cells and Ocular Neovascularizationmentioning

confidence: 99%

“…BMCs are affected by several risk factors like aging and are known to regulate the severity of ocular neovascularization formation. Aging BMCs are known to have age-related dysfunction, which may be associated with a more intense response to pro-vascularization factors, an increased number of cells distributed to their corresponding positions and an altered direction of differentiation, thereby enhancing the severity of ocular neovascularization [ 1 ]. In their earlier studies of CNV, Espinosa-Heidmann et al reported the effect of aging on neovascular remodeling [ 73 , 74 ].…”

Section: Risk Factors Affecting Bone Marrow-derived Cells’ Contributimentioning

confidence: 99%

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Bone marrow-derived cells in ocular neovascularization: contribution and mechanisms

et al. 2016

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Ocular neovascularization often leads to severe vision loss. The role of bone marrow-derived cells (BMCs) in the development of ocular neovascularization, and its significance, is increasingly being recognized. In this review, we discuss their contribution and the potential mechanisms that mediate the effect of BMCs on the progression of ocular neovascularization. The sequence of events by which BMCs participate in ocular neovascularization can be roughly divided into four phases, i.e., mobilization, migration, adhesion and differentiation. This process is delicately regulated and liable to be affected by multiple factors. Cytokines such as vascular endothelial growth factor, granulocyte colony-stimulating factor and erythropoietin are involved in the mobilization of BMCs. Studies have also demonstrated a key role of cytokines such as stromal cell-derived factor-1, tumor necrosis factor-α, as well as vascular endothelial growth factor, in regulating the migration of BMCs. The adhesion of BMCs is mainly regulated by vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and vascular endothelial cadherin. However, the mechanisms regulating the differentiation of BMCs are largely unknown at present. In addition, BMCs secrete cytokines that interact with the microenvironment of ocular neovascularization; their contribution to ocular neovascularization, especially choroidal neovascularization, can be aggravated by several risk factors. An extensive regulatory network is thought to modulate the role of BMCs in the development of ocular neovascularization. A comprehensive understanding of the involved mechanisms will help in the development of novel therapeutic strategies related to BMCs. In this review, we have limited the discussion to the recent progress in this field, especially the research conducted at our laboratory.

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“…Choroidal neovascularization involves both angiogenesis and vasculogenesis (recruitment and in situ differentiation of vascular endothelial cells from circulating bone marrow-derived cells) (Abu El-Asrar et al, 2011;Hou et al, 2011;Zhang et al, 2011). Vascular endothelial growth factor (VEGF) is pivotal in the pathogenesis of choroidal neovascularization, and plays an important role in the development of wet age-related macular degeneration (Bhutto et al, 2006;Huang et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐195a‐3p inhibits angiogenesis by targeting Mmp2 in murine mesenchymal stem cells

Gao

Sun

Gong

et al. 2016

Molecular Reproduction Devel

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MicroRNAs (miRNAs) modulate complex physiological and pathological processes, including the regulation of angiogenesis. Our previous study reported that bone marrow-derived mesenchymal stem cells (MSCs) are recruited into choroidal neovascularization lesions. miRNA-195 is highly expressed in MSCs, but its function remains unknown. In the present study, miR-195a-3p abundance was significantly decreased in hypoxia-treated murine MSCs; on the other hand, its overexpression reduced MSC proliferation and migration while increasing the activation of anti-angiogenic factor pigment epithelium-derived factor (PEDF). We further discovered that matrix metalloproteinase 2 (Mmp2) transcript is a target of miR-195a-3p, and that silencing Mmp2 phenocopied the reduced proliferation and migration of MSCs. The therapeutic potential of miR-195a-3p as an angiogenesis inhibitor was also demonstrated in a laser-induced choroidal neovascularization mouse model. These findings collectively indicate that miR-195a-3p is a negative modulator of angiogenesis, and could be used as an angiogenesis inhibitor. Mol. Reprod. Dev. 83: 413-423, 2016. © 2016 Wiley Periodicals, Inc.

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Bone Marrow-Derived Cells in Neovascular Age-Related Macular Degeneration: Contribution and Potential Application

Cited by 8 publications

References 47 publications

CXCR7/CXCR4/CXCL12 Axis Regulates the Proliferation, Migration, Survival and Tube Formation of Choroid-Retinal Endothelial Cells

CXCR7/CXCR4/CXCL12 Axis Regulates the Proliferation, Migration, Survival and Tube Formation of Choroid-Retinal Endothelial Cells

Bone marrow-derived cells in ocular neovascularization: contribution and mechanisms

MicroRNA‐195a‐3p inhibits angiogenesis by targeting Mmp2 in murine mesenchymal stem cells

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