The role of fucosylation in the promotion of endothelial progenitor cells in neovascularization and bone repair

Sun, Shengxuan; Liu, Zhenzhen; Zhou, Haibin; Li, Guoqiang; Li, Meng; Yao, Jiannan; Zhou, Tiantian; An, Guangyu; Wu, Qingyu; Dong, Ningzheng

doi:10.1016/j.biomaterials.2014.01.025

Cited by 7 publications

(3 citation statements)

References 46 publications

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“…Endothelial progenitor cells (EPCs) are bone marrow-derived stem cells, which have been recognized as angiogenic factors during bone healing (Keramaris et al, 2012 ; Sun et al, 2014 ). Obesity is associated with reduced expression of EPCs through different mechanisms and thereby decreases the rate of angiogenesis required for bone formation in the fracture sites (Chen Y. L. et al, 2012 ; Sun et al, 2014 ). Mice fed a high fat diet for 22 weeks expressed lower numbers of circulating as well as differentiated EPCs compared to mice on a high fat diet for 14 weeks (Chen Y. L. et al, 2012 ).…”

Section: Regulators Of Bone Formation and Resorptionmentioning

confidence: 99%

Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy

et al. 2016

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Obesity and osteoporosis are two alarming health disorders prominent among middle and old age populations, and the numbers of those affected by these two disorders are increasing. It is estimated that more than 600 million adults are obese and over 200 million people have osteoporosis worldwide. Interestingly, both of these abnormalities share some common features including a genetic predisposition, and a common origin: bone marrow mesenchymal stromal cells. Obesity is characterized by the expression of leptin, adiponectin, interleukin 6 (IL-6), interleukin 10 (IL-10), monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), macrophage colony stimulating factor (M-CSF), growth hormone (GH), parathyroid hormone (PTH), angiotensin II (Ang II), 5-hydroxy-tryptamine (5-HT), Advance glycation end products (AGE), and myostatin, which exert their effects by modulating the signaling pathways within bone and muscle. Chemical messengers (e.g., TNF-α, IL-6, AGE, leptins) that are upregulated or downregulated as a result of obesity have been shown to act as negative regulators of osteoblasts, osteocytes and muscles, as well as positive regulators of osteoclasts. These additive effects of obesity ultimately increase the risk for osteoporosis and muscle atrophy. The aim of this review is to identify the potential cellular mechanisms through which obesity may facilitate osteoporosis, muscle atrophy and bone fractures.

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Section: Regulators Of Bone Formation and Resorptionmentioning

confidence: 99%

Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy

et al. 2016

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“…Overexpression of fucosyltransferase in EPCs enhance EPC homing function and neovascularization in a mouse model of hind-limb ischemia via E-and P-selectin expression improvement [52]. As well, angiotensin converting enzyme 2 priming and overexpression, by lentivirus transduction, improved UCB-derived EPC migration and tube formation through upregulation of eNOS Q 8 and Nox pathways [53].…”

Section: Endothelial-like Vascular Progenitor Cellsmentioning

confidence: 98%

Regenerative Therapy and Immune Modulation Using Umbilical Cord Blood–Derived Cells

Damien

Allan

2015

Biology of Blood and Marrow Transplantation

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Since the first cord blood transplantation in 1988, umbilical cord blood has become an important option as a source of cells for hematopoietic transplantation. Beyond its role in regenerating the blood and immune systems to treat blood diseases and inherited metabolic disorders, the role of nonhematopoietic progenitor cells in cord blood has led to new and emerging uses of umbilical cord blood in regenerative therapy and immune modulation. In this review, we provide an update on the clinical and preclinical studies using cord blood-derived cells such as mesenchymal stromal cells, endothelial-like progenitor cells, and others. We also provide insight on the use of cord blood cells as vehicles for the delivery of therapeutic agents through gene therapy and microvesicle-associated strategies. Moreover, cord blood can provide essential reagents for regenerative applications. Clinical activity using cord blood cells is increasing rapidly and this review aims to provide an important update on the tremendous potential within this fast-moving field.

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“…Core fucosylated free oligosaccharides derived from maternal milk N -glycosylated proteins activate B cells via B cell receptor-mediated downstream signaling [ 95 ]. Several studies have revealed that fucosyltransferases and fucosylated proteins play positive roles in angiogenesis via the activation of fibroblasts, vascular endothelial cells, and endothelial progenitor cells [ 96 , 97 , 98 ]. In addition, the fucosylated glycans increase angiogenesis by interacting with galectin-12 or releasing angiogenic bFGF and VEGF [ 84 , 86 ].…”

Section: Human Milk Oligosaccharides and Angiogenesismentioning

confidence: 99%

Anti-Angiogenic Property of Free Human Oligosaccharides

et al. 2021

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Angiogenesis, a fundamental process in human physiology and pathology, has attracted considerable attention owing to its potential as a therapeutic strategy. Vascular endothelial growth factor (VEGF) and its receptor (VEGFR) are deemed major mediators of angiogenesis. To date, inhibition of the VEGF-A/VEGFR-2 axis has been an effective strategy employed in the development of anticancer drugs. However, some limitations, such as low efficacy and side effects, need to be addressed. Several drug candidates have been discovered, including small molecule compounds, recombinant proteins, and oligosaccharides. In this review, we focus on human oligosaccharides as modulators of angiogenesis. In particular, sialylated human milk oligosaccharides (HMOs) play a significant role in the inhibition of VEGFR-2-mediated angiogenesis. We discuss the structural features concerning the interaction between sialylated HMOs and VEGFR-2 as a molecular mechanism of anti-angiogenesis modulation and its effectiveness in vivo experiments. In the current state, extensive clinical trials are required to develop a novel VEGFR-2 inhibitor from sialylated HMOs.

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The role of fucosylation in the promotion of endothelial progenitor cells in neovascularization and bone repair

Cited by 7 publications

References 46 publications

Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy

Molecular Mechanisms of Obesity-Induced Osteoporosis and Muscle Atrophy

Regenerative Therapy and Immune Modulation Using Umbilical Cord Blood–Derived Cells

Anti-Angiogenic Property of Free Human Oligosaccharides

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