China
Africa
Explore chapters and articles related to this topic
Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Angiogenesis is the process underlying the formation and development of new blood vessels vital for the growth and development of new cells, as in wound healing. However, it also plays an important role in tumor growth, development, and metastasis, as it facilitates the transport of oxygen and nutrients to a growing tumor and the removal of waste products through the formation of a supporting vascular network. Angiogenesis is controlled by growth factors such as VEGF, TGF-α, TGF-β, TNF-α, angiogenin, IL-8, and the angiopoietins. One of the primary regulators of tumor angiogenesis is the pro-angiogenic factor VEGF, a potent endothelial cell-specific mitogen which stimulates endothelial cell growth originating in arteries, veins, and lymph drainage vessels (Figure 12.5).
Dopamine in the Immune and Hematopoietic Systems
Published in Nira Ben-Jonathan, Dopamine, 2020
Angiogenesis is a highly regulated process that takes place through two nonexclusive events of microvascular growth: sprouting or splitting [70]. Sprouting differs from splitting angiogenesis by forming entirely new vessels as opposed to splitting existing vessels. As illustrated in Figure 9.6, sprouting proceeds in several well-characterized stages. First, angiogenic factors [VEGF and fibroblast growth factor (FGF)], released from neighboring cells, bind to their respective receptors on endothelial cells and activate signal transduction pathways. Matrix metalloproteinases (MMPs), produced by the endothelial cells are then activated and degrade the extracellular matrix, enabling an escape of endothelial cells from the parental vessel walls. This is followed by their migration and proliferation. The integrins, expressed by endothelial cells, facilitate their adhesion to the extracellular matrix and the formation of solid sprouts that connect to neighboring vessels. Angiopoietin 1 (Ang-1), binding to Tie-2 receptors, stimulates pericyte recruitment and vessel stabilization. Final vessel maturation and stabilization necessitate additional morphological changes that include lumen formation and perfusion, network establishment, remodeling, and pruning to become full-fledged functional vessels.
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
The main angiogenic angiopoietin is Ang2, which causes vessel destabilization, initiation of angiogenesis, and transformation of capillaries into inflammatory venules, with increased leakiness and stickiness, in synergism with TNFα. Ang2 is expressed by endothelial cells near the VEGF-expressing epidermal keratinocytes in psoriasis lesions, and the vessel-stabilizing angiopoietin Ang1 is expressed by stromal cells in the vascularized papillary dermis of lesional skin. Their receptors Tie2 and Ang2 could also be upregulated in cultured dermal microvascular endothelial cell upon the addition of angiogenic factors like VEGF or FGF2. Successful antipsoriatic treatment was accompanied by a noticeable reduction of Ang2.
An overview of the molecular and clinical significance of the angiopoietin system in leukemia
Published in Journal of Receptors and Signal Transduction, 2023
Saeed Zaka Khosravi, Samira Molaei Ramshe, Mehdi Allahbakhshian Farsani, Mohammadreza Moonesi, Faroogh Marofi, Majid Farshdousti Hagh
The angiopoietins are a family of growth factors consisting of four ligands: angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), angiopoietin-3 (Ang-3), angiopoietin-4 (Ang-4), and their receptors: tyrosine kinase with immunoglobulin-like and EGF-like domains 1 (Tie-1) and Tek receptor tyrosine kinase-2 (Tie-2). Depending on the situation, this family engenders vessel stability and maturation, or vessel destabilization and regression. Studies have shown that Ang-1 and its antagonist, Ang-2, are the essential angiopoietins for angiogenesis. Ang-1 and Ang-2 exert their function by binding to Tie-2 receptor tyrosine kinase, which is located in the endothelium of the vascular system and some of the hematopoietic stem cells [9,10]. Ang-1 binds to and phosphorylates Tie-2 in endothelial cells, resulting in vascular stability. On the opposite side, Ang-2 blocks Ang-1/Tie-2 binding, which leads to angiogenesis by vessel destabilization in the presence of VEGF [11–13].
Serum VEGF and Ang-2 Levels in Infants Before and After Laser Treatment for Retinopathy of Prematurity
Published in Fetal and Pediatric Pathology, 2021
Xiaofeng Yang, Junping Wang, Chao Chen
The goal and standard of treatment of sight threatening ROP is ablative treatment of aberrant non-vascularized retina using laser photocoagulation. Laser therapy can reduce the production of VEGF by the immature retina and eliminate the abnormal growth of new vessels, preventing blindness in most cases with a failure rate of approximately 9.1% [6]. A meta-analysis indicated that laser treatment may be more efficacious than anti-VEGF treatment [7]. VEGF is a hypoxia inducible factor, and its expression can be upregulated by hypoxic and inflammatory stimuli. VEGF is an important component in this network and a major factor for the pathogenesis of ROP [8]. Angiopoietin2 (Ang-2) is a member of the angiopoietins (Ang). Ang-2 may cause vessel destabilization by acting as an antagonist for angiopoietin 1 (Ang-1) activation of Tie2 [5,9,10], and plays an important role by increasing angiogenesis in the pathogenesis of ROP [11,12]. Increased VEGF levels in serum [13] and eye are associated with ROP development, and higher VEGF serum level may be a predictor of ROP. However the relationship between Ang-2 serum levels and ROP has not been investigated.
Quantile-specific heritability of serum growth factor concentrations
Published in Growth Factors, 2021
VEGF stimulates endothelial cell nitric oxide and prostacyclin production (Hood et al. 1998; Neagoe et al. 2005), increases microvascular permeability (Bates et al. 2002), and prevents endothelial cell apoptosis (Lieb et al. 2009). It is inhibited by the circulating soluble form of the VEGFR1 receptor (sFlt-1) by direct sequestration (Shibuya 2006). Angiopoietin-2 promotes VEGF-induced neovascularization (Lieb et al. 2010). Both angiopoietin-2 and the soluble form of the sTie-2 (growth substances tyrosine kinase) receptor (Reusch et al. 2001) inhibit endothelial Ang-1/Tie-2 signaling (Peters 1998; Reusch et al. 2001), thereby attenuating the signal’s ability to prolong endothelial cell survival, maintainthe endothelium in a quiescent state, and facilitate new vessel maturation (Asahara et al. 1998). VEGF and HGF relate to improved endothelial function whereas sFlt-1 relates to endothelial dysfunction (Lieb et al. 2009).