Choroidal Neovascularization Is Provided by Bone Marrow Cells

Tomita, Minoru; Yamada, Haruhiko; Adachi, Yasushi; Cui, Yunze; Yamada, Eri; Higuchi, Akiko; Minamino, Keizo; Suzuki, Yasuhiko; Matsumura, Miyo; Ikehara, Susumu

doi:10.1634/stemcells.22-1-21

Cited by 52 publications

(34 citation statements)

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“…It has been reported that marrow-derived endothelial progenitor cells contribute to adult vasculogenesis (Tamura et al, 2004) and tumour angiogenesis (Rafii et al, 2002;Peters et al, 2005) by circulating through the vascular system and incorporating into the wall of newly formed vessels (Marchetti et al, 2002;Rafii and Lyden, 2003). Evidence that vasculogenesis is involved in neovascularisation has been found in studies on tumour vessels (Reyes et al, 2002), experimental retinopathy (Grant et al, 2002;Tomita et al, 2004;Butler et al, 2005), myocardial ischaemia (Kocher et al, 2001(Kocher et al, , 2006Botta et al, 2004), wound healing Crisa et al, 1999), and hindlimb ischaemia Kalka et al, 2000;Iwaguro et al, 2002). An important question that remains unanswered by the literature is whether circulating endothelial progenitor cells per se or their differentiated progeny are incorporated into the vascular wall .…”

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Systemic inhibition of tumour angiogenesis by endothelial cell-based gene therapy

et al. 2007

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Angiogenesis and post-natal vasculogenesis are two processes involved in the formation of new vessels, and both are essential for tumour growth and metastases. We isolated endothelial cells from human blood mononuclear cells by selective culture. These blood outgrowth cells expressed endothelial cell markers and responded correctly to functional assays. To evaluate the potential of blood outgrowth endothelial cells (BOECs) to construct functional vessels in vivo, NOD-SCID mice were implanted with Lewis lung carcinoma cells subcutaneously (s.c.). Blood outgrowth endothelial cells were then injected through the tail vein. Initial distribution of these cells occurred throughout the lung, liver, spleen, and tumour vessels, but they were only found in the spleen, liver, and tumour tissue 48 h after injection. By day 24, they were mainly found in the tumour vasculature. Tumour vessel counts were also increased in mice receiving BOEC injections as compared to saline injections. We engineered BOECs to deliver an angiogenic inhibitor directly to tumour endothelium by transducing them with the gene for human endostatin. These cells maintained an endothelial phenotype and decreased tumour vascularisation and tumour volume in mice. We conclude that BOECs have the potential for tumour-specific delivery of cancer gene therapy.

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Systemic inhibition of tumour angiogenesis by endothelial cell-based gene therapy

et al. 2007

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“…其造成的渗出、出血和增生等病理改变, 对眼部结构和功能的损害是引起视力障碍的重要原因 [1] . 目前对其发生机制的研究表明: 缺氧是诱导一些生长因子、整合素、蛋白酶表达上调的初始因素, 进而促进血管内皮细胞的增殖和迁移.…”

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“…目前对其发生机制的研究表明: 缺氧是诱导一些生长因子、整合素、蛋白酶表达上调的初始因素, 进而促进血管内皮细胞的增殖和迁移. 具体表现为: 视网膜色素上皮细胞能够表达血管内皮生长因子(VEGF)和基质细胞衍生因子定向趋化骨髓来源细胞, 并参与眼新生血管的发生发展 [1,2] , 而在高糖和缺氧刺激下这种作用更为明显 [3] . 因此, 通过抗血管化作用, 有望实现对该类疾病的治疗.…”

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Preparation of Biodegradable Poly(lactic-co-glycolic acid)/Polyethyle-ne Glycol Copolymer and Its Application as a Carrier for Pigment Epithelium-Derived Factor

赵俊颖¹,

朱艳吉²,

王岩岩³

et al. 2017

Chin. J. Org. Chem.

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“…The results of recent studies have provided evidence that endothelial progenitor cells (EPCs) may be major contributors to the development of CNV. [12][13][14][15][16][17] For example, experiments on laser-induced CNV in chimeric C57Bl/6 mice with bone marrow transplantation from green 22 The migration of EPCs into the subretinal space requires their mobilization from the bone marrow into the bloodstream and subsequent recruitment from the choroidal circulation into the subretinal space. Although the molecular pathways leading to the mobilization of EPCs from the bone marrow are not fully known, earlier studies demonstrated that several humoral factors, such as vascular endothelial growth factor, 23,24 erythropoietin, 25 adiponectin, 23 and stromal cellderived factor-1␣ 26 trigger the release of EPCs.…”

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Amyloid β Enhances Migration of Endothelial Progenitor Cells by Upregulating CX3CR1 in Response to Fractalkine, Which May Be Associated With Development of Choroidal Neovascularization

Wang

Ohno‐Matsui²,

Nakahama³

et al. 2011

ATVB

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Objective-Deposits that accumulate beneath retinal pigment epithelium, called drusen, are early signs of age-related macular degeneration (AMD). We have shown that amyloid ␤ (A␤) is present in drusen, and A␤ may be involved in AMD development. We have also shown that endothelial progenitor cells (EPCs) may contribute to the development of choroidal neovascularization (CNV). Thus, the purpose of this study was to investigate the role played by CX3CR1, a chemokine receptor, in EPC migration and CNV formation. Methods and Results-EPCs collected from human umbilical cords were found to express higher levels of CX3CR1 than human umbilical vein endothelial cells, and exposure of EPCs to A␤ caused further upregulation of CX3CR1. This upregulation was decreased by blocking fractalkine, a ligand of CX3CR1. Exposure of EPCs to fractalkine increased their migration, but pretreatment with A␤ enhanced the migration. The fractalkine-induced EPC migration was more inhibited by EPCs derived from CX3CR1 Ϫ/Ϫ mice than wild-type mice. The area of laser-induced CNV was significantly smaller in wild-type mice that received bone marrow transplantation from CX3CR1 Ϫ/Ϫ mice than in those that received transplantation from wild-type mice. Conclusion-These data suggest that A␤ enhances EPC migration through the upregulation of CX3CR1. This upregulation might play a role in development of CNV. (Arterioscler Thromb Vasc Biol. 2011;31:e11-e18.)Key Words: angiogenesis Ⅲ cell physiology Ⅲ vascular biology Ⅲ age-related macular degeneration Ⅲ endothelial progenitor cells A ge-related macular degeneration (AMD) is the leading cause of irreversible vision decrease in the elderly worldwide. [1][2][3][4] The decrease of vision results from geographical atrophy or choroidal neovascularization (CNV) in the macula of the eye. During the development of CNV, new vessels develop from the choroidal vessels and penetrate the thick matrix of the Bruch membrane and pass into the avascular subretinal space.Among the earliest signs of AMD are subretinal extracellular deposits, known as drusen, which accumulate beneath the retinal pigment epithelium (RPE). 5 Epidemiological studies have shown that the presence of many discrete or confluent drusen significantly increases the risk of developing CNV. 6,7 We have found that amyloid ␤ (A␤) peptides are present in drusen, and we have suggested that their presence is the primary stimulus for the development of AMD. 8 The A␤ peptides vary in length from 39 to 43 amino acid residues and are produced by the sequential proteolytic processing of precursors of amyloid proteins. 9 Interestingly, A␤ is the main component of the senile plaques found in the brains of Alzheimer's patients. 9 -11 The results of our study on senescent neprilysin gene-disrupted mice that lack the A␤-degrading enzyme showed that there was a significant increase in the deposition of A␤ in the subretinal space. 8 This is relevant to this study because these mice developed several characteristics of human eyes at the early stage AMD, although they...

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Choroidal Neovascularization Is Provided by Bone Marrow Cells

Abstract: Choroidal neovascularization (CNV) is a known cause of age-related macular degeneration (ARMD).

Cited by 52 publications

References 38 publications

Systemic inhibition of tumour angiogenesis by endothelial cell-based gene therapy

Systemic inhibition of tumour angiogenesis by endothelial cell-based gene therapy

Preparation of Biodegradable Poly(lactic-co-glycolic acid)/Polyethyle-ne Glycol Copolymer and Its Application as a Carrier for Pigment Epithelium-Derived Factor

Amyloid β Enhances Migration of Endothelial Progenitor Cells by Upregulating CX3CR1 in Response to Fractalkine, Which May Be Associated With Development of Choroidal Neovascularization

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