Angiopoietin 2 promotes angiogenesis in tissue-engineered bone and improves repair of bone defects by inducing autophagy

Yin, Jian; Gong, Ge; Sun, Chao; Yin, Zhaoyang; Zhu, Chao; Wang, Bin; Hu, Qin; Zhu, Yizhi; Liu, Xinhui

doi:10.1016/j.biopha.2018.06.078

Cited by 33 publications

(25 citation statements)

References 21 publications

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“…Exogenous Ang2 administration led to the production of catabolic proteases and a decrease of aggrecan and collagen II levels, highlighting Ang2 as a therapeutic target for intervertebral disc degeneration [108]. In the bone marrow, high concentrations of Ang2 enhanced autophagy and promoted vascularization and bone defect repair on a hydroxyapatite/collagen scaffold in rabbits [109]. Similar to VEGF, the plasma Ang2 concentration is dependent on the Ang2 concentration in the bone marrow.…”

Section: Role Of Ang2 In Diseasementioning

confidence: 99%

Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology

Akwii

Sajib

Zahra

et al. 2019

Cells

354

270

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Angiopoietins 1–4 (Ang1–4) represent an important family of growth factors, whose activities are mediated through the tyrosine kinase receptors, Tie1 and Tie2. The best characterized are angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2). Ang1 is a potent angiogenic growth factor signaling through Tie2, whereas Ang2 was initially identified as a vascular disruptive agent with antagonistic activity through the same receptor. Recent data demonstrates that Ang2 has context-dependent agonist activities. Ang2 plays important roles in physiological processes and the deregulation of its expression is characteristic of several diseases. In this review, we summarize the activity of Ang2 on blood and lymphatic endothelial cells, its significance in human physiology and disease, and provide a current view of the molecular signaling pathways regulated by Ang2 in endothelial cells.

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Section: Role Of Ang2 In Diseasementioning

confidence: 99%

Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology

Akwii

Sajib

Zahra

et al. 2019

Cells

354

270

View full text Add to dashboard Cite

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“…VEGF (like in animals) and PGF (reported here for the 1st time) showed increased expression only at the late stage. Both of these pathways are believed to be upregulated during bone repair [38] VEGFs by promoting neo-angiogenesis while, angiopoietin 1 and 2 support the formation of larger vessel structures and the development of collateral branches from existing vessels [39] or as shown more recently, via an autophagy-related mechanism [40]. Other growth factors such as PDGF and the TGF-betas were reported in late stages in animals (hard callus) and showed similar steady low increase in expression over time in humans for TGF-beta2 (no change in TGF-beta1) but a reduction followed by increase for PDGF.…”

Section: Discussionmentioning

confidence: 99%

Dynamics of Early Signalling Events during Fracture Healing and Potential Serum Biomarkers of Fracture Non-Union in Humans

Burska

Giannoudis

Tan

et al. 2020

JCM

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To characterise the dynamic of events during the early phases of fracture repair in humans, we investigated molecular events using gene expression profiling of bone fragments from the fracture site at different time points after trauma and immune/stromal cells recruitment at the fracture site using flow cytometry. Bone and inflammatory markers were expressed at low levels at homeostasis, while transcripts for bone constituent proteins were consistently detected at higher levels. Early after fracture (range 2–4 days), increased expression of CXCL12, suggested recruitment of immune cells associated with a change in the balance of degradation enzymes and their inhibitors. At intermediate time after fracture (4–8 days), we observed high expression of inflammatory cytokines (IL1-beta, IL6), CCL2, the T-cell activation marker CD69. Late after fracture (8–14 days), high expression of factors co-operating towards the regulation of bone turnover was detected. We identified potential soluble factors and explored circulating levels in patients for whom a union/non-union (U/NU) outcome was known. This showed a clear difference for PlGF (p = 0.003) at day 1. These findings can inform future studies further investigating the cascade of molecular events following fractures and for the prediction of fracture non-union.

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“…143 However, another protein from the BMP family, BMP-7, induces early graft remodeling by stimulating blood vessel formation and osteoclastic activity, as well as the expression of angiogenic and inflammatory cytokines. 134,144 Furthermore, proangiogenic growth factors and compounds, which may be used in bone tissue engineering applications, are insulin-like growth factor-1, 145 hepatocyte growth factor, 146 sphingosine 1-phosphate 147 and its receptor agonist FTY720, 148,149 angiopoietin-2, 150 plasma factor XIII, 151 G-CSF, 84 the glycoprotein fibrinogen, 152 and PRP, which contains a variety of cytokines (i.e., platelet-derived growth factor, TGF-b, and epidermal growth factor). [153][154][155][156] Of note, the local application of clinically approved drugs at the bone defect site, such as simvastatin, 157,158 rosuvastatin, 159 desferrioxamine, [160][161][162][163] and even antibiotics like minocycline, 164 has also beneficial effects on vascularization and bone formation.…”

Section: Local Growth Factor-based Vascularization Strategiesmentioning

confidence: 99%

Vascularization Strategies in the Prevention of Nonunion Formation

Menger

Laschke

Orth

et al. 2021

Tissue Engineering Part B: Reviews

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Delayed healing and nonunion formation are major challenges in orthopedic surgery, which require the development of novel treatment strategies. Vascularization is considered one of the major prerequisites for successful bone healing, providing an adequate nutrient supply and allowing the infiltration of progenitor cells to the fracture site. Hence, during the last decade, a considerable number of studies have focused on the evaluation of vascularization strategies to prevent or to treat nonunion formation. These involve (1) biophysical applications, (2) systemic pharmacological interventions, and (3) tissue engineering, including sophisticated scaffold materials, local growth factor delivery systems, cell-based techniques, and surgical vascularization approaches. Accumulating evidence indicates that in nonunions, these strategies are indeed capable of improving the process of bone healing. The major challenge for the future will now be the translation of these strategies into clinical practice to make them accessible for the majority of patients. If this succeeds, these vascularization strategies may markedly reduce the incidence of nonunion formation.

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Angiopoietin 2 promotes angiogenesis in tissue-engineered bone and improves repair of bone defects by inducing autophagy

Cited by 33 publications

References 21 publications

Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology

Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology

Dynamics of Early Signalling Events during Fracture Healing and Potential Serum Biomarkers of Fracture Non-Union in Humans

Vascularization Strategies in the Prevention of Nonunion Formation

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