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Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical...
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Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biological Factors".

Deadline for manuscript submissions: closed (30 December 2020) | Viewed by 52780

Special Issue Editor

Dr. Jody Jonathan Haigh

E-Mail Website
Guest Editor
1. Department of Pharmacology and Therapeutics, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada
2. CancerCare Manitoba Research Institute, Winnipeg, MB, Canada
Interests: cancer biology; cell fate engineering; epigenetics; hematopoiesis; in vivo disease modeling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Vascular Endothelial Growth Factor (VEGF or VEGF-A), since its initial discovery in the late 1980s by Napoleone Ferrara and colleagues, has been one of the most studied growth factors in history, with more than 76,000 publications to date. The main reason for such avid interest in VEGF is based on its critical importance in blood vessel development, organogenesis, tissue homeostasis, as well as pathological processes associated with cancer progression and cardiovascular and neuronal associated diseases, to name just a few. Initial gene targeting studies in 1996 demonstrated that VEGF was one of the first documented haploinsufficient lethalities associated with loss of a single allele, thereby underscoring (1) how threshold levels of this important growth factor are essential for normal vascular development and (2) the importance of the vasculature for normal embryogenesis and organ development. Over the last 3 decades, work on VEGF and its family members (VEGF-A-E, PlGF) as well as its main signalling receptors (VEGFR1-3) and co-receptors (Nrp1-2) has not only shed light on the complexity of vascular patterning and specification but has also led to the development of novel targeting agents that hold great promise for the treatment of various human diseases. In particular excessive VEGF secretion and signalling has been associated with enhanced tumour growth and metastasis as well as ocular diseases such as retinopathy of prematurity, diabetic retinopathy and amacular degeneration. Development and FDA approval of a humanized monoclonal antibody against VEGF termed Bevacizumab has shown significant promise in the treatment of these diseases. However, given the biological complexity of the signaling molecules involved in vascular biology and cellular crosstalk, the development of combination therapies that can be used in synergy with VEGF signaling inhibition is warranted in order to develop more efficacious treatments and avoid resistance mechanisms particularly evident in cancer.

The purpose of this Special Issue of Biomolecules is to bring together both original papers and review articles that encompass the complexity of VEGF biology and advancements in our understanding of VEGF signalling crosstalk in both developmental processes, organ homeostasis and disease progression, with a particular focus on cancer biology and novel combination therapy approaches.

Dr. Jody Jonathan Haigh
Guest Editor

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Keywords

  • VEGF/VEGFR signalling
  • Signalling Crosstalk
  • Angiogenesis/vasculogenesis
  • Organogenesis
  • Tissue homeostasis
  • Anti-angiogenesis therapies
  • Cancer combination therapies

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Published Papers (10 papers)

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Research

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15 pages, 16201 KiB  
Article
The Ablation of VEGFR-1 Signaling Promotes Pressure Overload-Induced Cardiac Dysfunction and Sudden Death
by Annakaisa Tirronen, Nicholas L. Downes, Jenni Huusko, Johanna P. Laakkonen, Tomi Tuomainen, Pasi Tavi, Marja Hedman and Seppo Ylä-Herttuala
Biomolecules 2021, 11(3), 452; https://doi.org/10.3390/biom11030452 - 17 Mar 2021
Cited by 5 | Viewed by 3358
Abstract
Molecular mechanisms involved in cardiac remodelling are not fully understood. To study the role of vascular endothelial growth factor receptor 1 (VEGFR-1) signaling in left ventricular hypertrophy (LVH) and heart failure, we used a mouse model lacking the intracellular VEGFR-1 tyrosine kinase domain [...] Read more.
Molecular mechanisms involved in cardiac remodelling are not fully understood. To study the role of vascular endothelial growth factor receptor 1 (VEGFR-1) signaling in left ventricular hypertrophy (LVH) and heart failure, we used a mouse model lacking the intracellular VEGFR-1 tyrosine kinase domain (VEGFR-1 TK−/−) and induced pressure overload with angiotensin II infusion. Using echocardiography (ECG) and immunohistochemistry, we evaluated pathological changes in the heart during pressure overload and measured the corresponding alterations in expression level and phosphorylation of interesting targets by deep RNA sequencing and Western blot, respectively. By day 6 of pressure overload, control mice developed significant LVH whereas VEGFR-1 TK−/− mice displayed a complete absence of LVH, which correlated with significantly increased mortality. At a later time point, the cardiac dysfunction led to increased ANP and BNP levels, atrial dilatation and prolongation of the QRSp duration as well as increased cardiomyocyte area. Immunohistochemical analyses showed no alterations in fibrosis or angiogenesis in VEGFR-1 TK−/− mice. Mechanistically, the ablation of VEGFR-1 signaling led to significantly upregulated mTOR and downregulated PKCα phosphorylation in the myocardium. Our results show that VEGFR-1 signaling regulates the early cardiac remodelling during the compensatory phase of pressure overload and increases the risk of sudden death. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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13 pages, 1652 KiB  
Article
Activated Protein C (APC) and 3K3A-APC-Induced Regression of Choroidal Neovascularization (CNV) Is Accompanied by Vascular Endothelial Growth Factor (VEGF) Reduction
by Tami Livnat, Yehonatan Weinberger, José A. Fernández, Alaa Bashir, Gil Ben-David, Dahlia Palevski, Sarina Levy-Mendelovich, Gili Kenet, Ivan Budnik, Yael Nisgav, John H. Griffin and Dov Weinberger
Biomolecules 2021, 11(3), 358; https://doi.org/10.3390/biom11030358 - 26 Feb 2021
Cited by 6 | Viewed by 2444
Abstract
The activated protein C (APC) ability to inhibit choroidal neovascularization (CNV) growth and leakage was recently shown in a murine model. A modified APC, 3K3A-APC, was designed to reduce anticoagulant activity while maintaining full cytoprotective properties, thus diminishing bleeding risk. We aimed to [...] Read more.
The activated protein C (APC) ability to inhibit choroidal neovascularization (CNV) growth and leakage was recently shown in a murine model. A modified APC, 3K3A-APC, was designed to reduce anticoagulant activity while maintaining full cytoprotective properties, thus diminishing bleeding risk. We aimed to study the ability of 3K3A-APC to induce regression of CNV and evaluate vascular endothelial growth factor (VEGF) role in APC’s activities in the retina. CNV was induced by laser photocoagulation on C57BL/6J mice. APC and 3K3A-APC were injected intravitreally after verification of CNV presence. CNV volume and vascular penetration were evaluated on retinal pigmented epithelium (RPE)-choroid flatmount by fluorescein isothiocyanate (FITC)-dextran imaging. VEGF levels were measured using immunofluorescence anti-VEGF staining. We found that 3K3A-APC induced regression of pre-existing CNV. VEGF levels, measured in the CNV lesion sites, significantly decreased upon APC and 3K3A-APC treatment. Reduction in VEGF was sustained 14 days post a single APC injection. As 3K3A-APC retained APCs’ activities, we conclude that the anticoagulant properties of APC are not mandatory for APC activities in the retina and that VEGF reduction may contribute to the protective effects of APC and 3K3A-APC. Our results highlight the potential use of 3K3A-APC as a novel treatment for CNV and other ocular pathologies. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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13 pages, 2011 KiB  
Article
The Influence of Melatonin and Light on VEGF Secretion in Primary RPE Cells
by Alexa Klettner, Miriam Kampers, Daniela Töbelmann, Johann Roider and Manuela Dittmar
Biomolecules 2021, 11(1), 114; https://doi.org/10.3390/biom11010114 - 16 Jan 2021
Cited by 20 | Viewed by 3311
Abstract
(1) Background: Retinal pigment epithelial cells (RPE) cells constitutively secrete vascular endothelial growth factor (VEGF) in the retina, protecting the neuronal cells and the choroid. Increased VEGF secretion, however, can result in neovascularization and edema. Many factors regulate VEGF secretion. In this study, [...] Read more.
(1) Background: Retinal pigment epithelial cells (RPE) cells constitutively secrete vascular endothelial growth factor (VEGF) in the retina, protecting the neuronal cells and the choroid. Increased VEGF secretion, however, can result in neovascularization and edema. Many factors regulate VEGF secretion. In this study, we investigated the effect of external stimuli in relation to diurnal rhythm on constitutive VEGF secretion. (2) Methods: Single-eye RPE cell culture was prepared from porcine eyes. RPE cells were cultured in darkness, treated with daylight or room light, and treated with melatonin at different time frames, either respectively or in combination. Supernatants were collected and VEGF content evaluated using ELISA. Expression of the clock protein BMAL1 was evaluated with Western blot. (3) Results: VEGF secretion of the RPE shows a diurnal rhythm. While the rhythm is not influenced by either light or melatonin, the amount of secreted VEGF can be increased by nocturnal melatonin, especially in combination with morning daylight. These findings disclose another layer of VEGF regulation in the retina. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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10 pages, 1666 KiB  
Article
Molecular Targeting of VEGF with a Suramin Fragment–DOCA Conjugate by Mimicking the Action of Low Molecular Weight Heparins
by Jooho Park, Tae-Bong Kang, Ji-Hong Lim and Hyung-Sik Won
Biomolecules 2021, 11(1), 46; https://doi.org/10.3390/biom11010046 - 31 Dec 2020
Cited by 4 | Viewed by 2801
Abstract
Molecular targeting of growth factors has shown great therapeutic potential in pharmaceutical research due to their roles in pathological conditions. In the present study, we developed a novel suramin fragment and deoxycholic acid conjugate (SFD) that exhibited the potential to bind to the [...] Read more.
Molecular targeting of growth factors has shown great therapeutic potential in pharmaceutical research due to their roles in pathological conditions. In the present study, we developed a novel suramin fragment and deoxycholic acid conjugate (SFD) that exhibited the potential to bind to the heparin-binding site (HBD) of vascular endothelial growth factor (VEGF) and to inhibit its pathogenic action for the first time. Notably, SFD was optimally designed for binding to the HBD of VEGF using the naphthalenetrisulfonate group, allowing to observe its excellent binding efficacy in a surface plasmon resonance (SPR) study, showing remarkable binding affinity (KD = 3.8 nM) as a small molecule inhibitor. In the tubular formation assay, it was observed that SFD could bind to HBD and exhibit antiangiogenic efficacy by inhibiting VEGF, such as heparins. The cellular treatment of SFD resulted in VEGF-inhibitory effects in human umbilical vein endothelial cells (HUVECs). Therefore, we propose that SFD can be employed as a novel drug candidate to inhibit the pathophysiological action of VEGF in diseases. Consequently, SFD, which has a molecular structure optimized for binding to HBD, is put forward as a new chemical VEGF inhibitor. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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11 pages, 1193 KiB  
Article
Does Cysteine Rule (CysR) Complete the CendR Principle? Increase in Affinity of Peptide Ligands for NRP-1 Through the Presence of N-Terminal Cysteine
by Anna K. Puszko, Piotr Sosnowski, Françoise Raynaud, Olivier Hermine, Gérard Hopfgartner, Yves Lepelletier and Aleksandra Misicka
Biomolecules 2020, 10(3), 448; https://doi.org/10.3390/biom10030448 - 13 Mar 2020
Cited by 9 | Viewed by 3303
Abstract
The structure-activity relationship of branched H-Lys(hArg)-Dab-Dhp-Arg-OH sequence analogues, modified with Cys-Asp or Cys at N-terminal amino acids (Lys, hArg), in VEGF-A165/Neuropilin-1 complex inhibition is presented. The addition of Cys residue led to a 100-fold decrease in the IC [...] Read more.
The structure-activity relationship of branched H-Lys(hArg)-Dab-Dhp-Arg-OH sequence analogues, modified with Cys-Asp or Cys at N-terminal amino acids (Lys, hArg), in VEGF-A165/Neuropilin-1 complex inhibition is presented. The addition of Cys residue led to a 100-fold decrease in the IC50 value, compared to the parent peptide. The change occurred regardless of coupling Cys to the free N-terminal amino group present in the main or the side chain. A few analogues extended by the attachment of Cys at the N-terminus of several potent NRP-1 peptide ligands documented in the literature are also presented. In all studied cases, the enhancement of inhibitory properties after the addition of Cys at the N-terminus is observed. It is particularly evident for the tetrapeptide derived from the C-terminus of VEGF-A165 (KPRR), suggesting that extending the K/RXXK/R motif (CendR) with the Cys moiety can significantly improve affinity to NRP-1 of CendR peptides. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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Review

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18 pages, 1756 KiB  
Review
Neuropilin 1 Regulation of Vascular Permeability Signaling
by Alison Domingues and Alessandro Fantin
Biomolecules 2021, 11(5), 666; https://doi.org/10.3390/biom11050666 - 29 Apr 2021
Cited by 27 | Viewed by 4446
Abstract
The vascular endothelium acts as a selective barrier to regulate macromolecule exchange between the blood and tissues. However, the integrity of the endothelium barrier is compromised in an array of pathological settings, including ischemic disease and cancer, which are the leading causes of [...] Read more.
The vascular endothelium acts as a selective barrier to regulate macromolecule exchange between the blood and tissues. However, the integrity of the endothelium barrier is compromised in an array of pathological settings, including ischemic disease and cancer, which are the leading causes of death worldwide. The resulting vascular hyperpermeability to plasma molecules as well as leukocytes then leads to tissue damaging edema formation and inflammation. The vascular endothelial growth factor A (VEGFA) is a potent permeability factor, and therefore a desirable target for impeding vascular hyperpermeability. However, VEGFA also promotes angiogenesis, the growth of new blood vessels, which is required for reperfusion of ischemic tissues. Moreover, edema increases interstitial pressure in poorly perfused tumors, thereby affecting the delivery of therapeutics, which could be counteracted by stimulating the growth of new functional blood vessels. Thus, targets must be identified to accurately modulate the barrier function of blood vessels without affecting angiogenesis, as well as to develop more effective pro- or anti-angiogenic therapies. Recent studies have shown that the VEGFA co-receptor neuropilin 1 (NRP1) could be playing a fundamental role in steering VEGFA-induced responses of vascular endothelial cells towards angiogenesis or vascular permeability. Moreover, NRP1 is involved in mediating permeability signals induced by ligands other than VEGFA. This review therefore focuses on current knowledge on the role of NRP1 in the regulation of vascular permeability signaling in the endothelium to provide an up-to-date landscape of the current knowledge in this field. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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16 pages, 1060 KiB  
Review
Role of Vascular Endothelial Growth Factor (VEGF) in Human Embryo Implantation: Clinical Implications
by Xi Guo, Hong Yi, Tin Chiu Li, Yu Wang, Huilin Wang and Xiaoyan Chen
Biomolecules 2021, 11(2), 253; https://doi.org/10.3390/biom11020253 - 10 Feb 2021
Cited by 89 | Viewed by 11337
Abstract
Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the [...] Read more.
Vascular endothelial growth factor (VEGF) is a well-known angiogenic factor that plays a critical role in various physiological and pathological processes. VEGF also contributes to the process of embryo implantation by enhancing embryo development, improving endometrial receptivity, and facilitating the interactions between the developing embryo and the endometrium. There is a correlation between the alteration of VEGF expression and reproductive failure, including recurrent implantation failure (RIF) and recurrent miscarriage (RM). In order to clarify the role of VEGF in embryo implantation, we reviewed recent literature concerning the expression and function of VEGF in the reproductive system around the time of embryo implantation and we provide a summary of the findings reported so far. We also explored the effects and the possible underlying mechanisms of action of VEGF in embryo implantation. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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13 pages, 7084 KiB  
Review
Exploring the Intracrine Functions of VEGF-A
by Sophie Wiszniak and Quenten Schwarz
Biomolecules 2021, 11(1), 128; https://doi.org/10.3390/biom11010128 - 19 Jan 2021
Cited by 54 | Viewed by 7806
Abstract
Vascular endothelial growth factor A (VEGF-A or VEGF) is a highly conserved secreted signalling protein best known for its roles in vascular development and angiogenesis. Many non-endothelial roles for VEGF are now established, with the discovery that VEGF and its receptors VEGFR1 and [...] Read more.
Vascular endothelial growth factor A (VEGF-A or VEGF) is a highly conserved secreted signalling protein best known for its roles in vascular development and angiogenesis. Many non-endothelial roles for VEGF are now established, with the discovery that VEGF and its receptors VEGFR1 and VEGFR2 are expressed in many non-vascular cell-types, as well as various cancers. In addition to secreted VEGF binding to its receptors in the extracellular space at the cell membrane (i.e., in a paracrine or autocrine mode), intracellularly localised VEGF is emerging as an important signalling molecule regulating cell growth, survival, and metabolism. This intracellular mode of signalling has been termed “intracrine”, and refers to the direct action of a signalling molecule within the cell without being secreted. In this review, we describe examples of intracrine VEGF signalling in regulating cell growth, differentiation and survival, both in normal cell homeostasis and development, as well as in cancer. We further discuss emerging evidence for the molecular mechanisms underpinning VEGF intracrine function, as well as the implications this intracellular mode of VEGF signalling may have for use and design of anti-VEGF cancer therapeutics. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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27 pages, 1807 KiB  
Review
Vascular Endothelial Growth Factor: A Translational View in Oral Non-Communicable Diseases
by Sven Niklander, María José Bordagaray, Alejandra Fernández and Marcela Hernández
Biomolecules 2021, 11(1), 85; https://doi.org/10.3390/biom11010085 - 12 Jan 2021
Cited by 21 | Viewed by 4928
Abstract
Vascular endothelial growth factors (VEGFs) are vital regulators of angiogenesis that are expressed in response to soluble mediators, such as cytokines and growth factors. Their physiologic functions include blood vessel formation, regulation of vascular permeability, stem cell and monocyte/macrophage recruitment and maintenance of [...] Read more.
Vascular endothelial growth factors (VEGFs) are vital regulators of angiogenesis that are expressed in response to soluble mediators, such as cytokines and growth factors. Their physiologic functions include blood vessel formation, regulation of vascular permeability, stem cell and monocyte/macrophage recruitment and maintenance of bone homeostasis and repair. In addition, angiogenesis plays a pivotal role in chronic pathologic conditions, such as tumorigenesis, inflammatory immune diseases and bone loss. According to their prevalence, morbidity and mortality, inflammatory diseases affecting periodontal tissues and oral cancer are relevant non-communicable diseases. Whereas oral squamous cell carcinoma (OSCC) is considered one of the most common cancers worldwide, destructive inflammatory periodontal diseases, on the other hand, are amongst the most prevalent chronic inflammatory conditions affecting humans and also represent the main cause of tooth loss in adults. In the recent years, while knowledge regarding the role of VEGF signaling in common oral diseases is expanding, new potential translational applications emerge. In the present narrative review we aim to explore the role of VEGF signaling in oral cancer and destructive periodontal inflammatory diseases, with emphasis in its translational applications as potential biomarkers and therapeutic targets. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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25 pages, 2374 KiB  
Review
Structural Basis for Vascular Endothelial Growth Factor Receptor Activation and Implications for Disease Therapy
by Faheem Shaik, Gary A. Cuthbert, Shervanthi Homer-Vanniasinkam, Stephen P. Muench, Sreenivasan Ponnambalam and Michael A. Harrison
Biomolecules 2020, 10(12), 1673; https://doi.org/10.3390/biom10121673 - 15 Dec 2020
Cited by 55 | Viewed by 7726
Abstract
Vascular endothelial growth factors (VEGFs) bind to membrane receptors on a wide variety of cells to regulate diverse biological responses. The VEGF-A family member promotes vasculogenesis and angiogenesis, processes which are essential for vascular development and physiology. As angiogenesis can be subverted in [...] Read more.
Vascular endothelial growth factors (VEGFs) bind to membrane receptors on a wide variety of cells to regulate diverse biological responses. The VEGF-A family member promotes vasculogenesis and angiogenesis, processes which are essential for vascular development and physiology. As angiogenesis can be subverted in many disease states, including tumour development and progression, there is much interest in understanding the mechanistic basis for how VEGF-A regulates cell and tissue function. VEGF-A binds with high affinity to two VEGF receptor tyrosine kinases (VEGFR1, VEGFR2) and with lower affinity to co-receptors called neuropilin-1 and neuropilin-2 (NRP1, NRP2). Here, we use a structural viewpoint to summarise our current knowledge of VEGF-VEGFR activation and signal transduction. As targeting VEGF-VEGFR activation holds much therapeutic promise, we examine the structural basis for anti-angiogenic therapy using small-molecule compounds such as tyrosine kinase inhibitors that block VEGFR activation and downstream signalling. This review provides a rational basis towards reconciling VEGF and VEGFR structure and function in developing new therapeutics for a diverse range of ailments. Full article
(This article belongs to the Special Issue Vascular Endothelial Growth Factor (VEGF): From Basic Mechanisms to Clinical Significance and Drug Development)
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