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Advances in the Angiogenic Field
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Advances in the Angiogenic Field

A special issue of International Journal of Translational Medicine (ISSN 2673-8937).

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 18558

Special Issue Editors

Prof. Dr. Stefania Mitola

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy
Interests: angiogenesis; membrane receptor; tumors; imaging; metabolism; bioscaffold for tissue regeneration
Special Issues, Collections and Topics in MDPI journals
Dr. Michela Corsini

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy
Interests: angiogenesis; ECM; imaging; animal models; tumors
Special Issues, Collections and Topics in MDPI journals
Dr. Cosetta Ravelli

E-Mail Website
Guest Editor
Department of Molecular and Translational Medicine, University of Brescia, 25123 Brescia, Italy
Interests: angiogenesis; ECM; advanced imaging technologies; membrane receptor dynamics; tumors

Special Issue Information

Dear Colleagues,

Blood vessels are a prerequisite for normal development, tissue growth, and repair as they provide nutrients, remove waste products, and transport cells to distant sites. Blood vessels arise through two processes: vasculogenesis and angiogenesis. Due to its crucial role in physiological and pathological conditions, angiogenesis has been extensively studied and is now recognized as a promising therapeutic target in various pathological settings. Furthermore, blood vessels are essential in developing engineered tissues for regenerative medicine. Despite their quiescent state, ECs retain their angiogenesis competency since they can respond to an angiogenic stimulus imbalance. Excessive or insufficient neovascularization is characteristic of several pathologies. Consequently, a fine regulation of angiogenesis is necessary for human physiology to maintain homeostasis. Recently technological advancements have allowed a deep understanding of the mechanisms supporting angiogenic events, EC crosstalk with the microenvironment, and identifying new therapeutic targets.

This Special Issue aims to summarize the current knowledge and cutting-edge research on angiogenesis in human diseases. Translational studies are particularly welcome.

Prof. Dr. Stefania Mitola
Dr. Michela Corsini
Dr. Cosetta Ravelli
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Translational Medicine is an international peer-reviewed open access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • endothelial cell
  • growth factors
  • microenvironment
  • differentiation
  • therapeutically targets
  • inflammation

Published Papers (5 papers)

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Research

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15 pages, 2970 KiB  
Article
Hypoxia Increases Nitric Oxide-Dependent Inhibition of Angiogenic Growth
by Cristina Arce, Diana Vicente, Fermí Monto, Laura González, Cristina Nuñez, Víctor M. Victor, Francesc Jiménez-Altayó and Pilar D’Ocon
Int. J. Transl. Med. 2021, 1(3), 366-380; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1030022 - 08 Dec 2021
Viewed by 2361
Abstract
Nitric oxide (NO) is a proangiogenic factor acting through the soluble guanylate cyclase (sGC) pathway. However, angiogenic growth increases energy demand, which may be hampered by NO inhibition of cytochrome c oxidase (CcO). Then, NO activity would be the balanced result of sGC [...] Read more.
Nitric oxide (NO) is a proangiogenic factor acting through the soluble guanylate cyclase (sGC) pathway. However, angiogenic growth increases energy demand, which may be hampered by NO inhibition of cytochrome c oxidase (CcO). Then, NO activity would be the balanced result of sGC activation (pro-angiogenic) and CcO inhibition (anti-angiogenic). NO activity in a rat and eNOS−/− mice aortic ring angiogenic model and in a tube formation assay (human aortic endothelial cells) were analyzed in parallel with mitochondrial O2 consumption. Studies were performed with NO donor (DETA-NO), sGC inhibitor (ODQ), and NOS or nNOS inhibitors (L-NAME or SMTC, respectively). Experiments were performed under different O2 concentrations (0–21%). Key findings were: (i) eNOS-derived NO inhibits angiogenic growth by a mechanism independent on sGC pathway and related to inhibition of mitochondrial O2 consumption; (ii) NO inhibition of the angiogenic growth is more evident in hypoxic vessels; (iii) in the absence of eNOS-derived NO, the modulation of angiogenic growth, related to hypoxia, disappears. Therefore, NO, but not lower O2 levels, decreases the angiogenic response in hypoxia through competitive inhibition of CcO. This anti-angiogenic activity could be a promising target to impair pathological angiogenesis in hypoxic conditions, as it occurs in tumors or ischemic diseases. Full article
(This article belongs to the Special Issue Advances in the Angiogenic Field)
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22 pages, 8813 KiB  
Article
Crosstalk of Endothelial and Mesenchymal Stromal Cells under Tissue-Related O2
by Olga Zhidkova, Elena Andreeva, Mariia Ezdakova and Ludmila Buravkova
Int. J. Transl. Med. 2021, 1(2), 116-136; https://doi.org/10.3390/ijtm1020009 - 07 Sep 2021
Cited by 2 | Viewed by 3229
Abstract
Mesenchymal stromal cells (MSCs) are considered a valuable tool for cell therapy. After systemic administration, the outcome of MSCs and endothelial cells (ECs) interactions strongly depend on the local microenvironment and tissue O2 levels in particular. In vitro analysis of EC effects [...] Read more.
Mesenchymal stromal cells (MSCs) are considered a valuable tool for cell therapy. After systemic administration, the outcome of MSCs and endothelial cells (ECs) interactions strongly depend on the local microenvironment and tissue O2 levels in particular. In vitro analysis of EC effects on MSC regenerative potential in co-culture was performed after short-term interaction at “physiological” hypoxia (5% O2) and acute hypoxic stress (0.1% O2). At 5% O2, MSCs retained stromal phenotype and CFU-f numbers, osteogenic RUNX2 was upregulated. A shift in the expression of adhesion molecules, and an increase in transcription/synthesis of IL-6, IL-8 contributed to facilitation of directed migration of MSCs. In the presence of MSCs, manifestations of oxidative stress in ECs were attenuated, and a decrease in adhesion of PBMCs to TNF-α-activated ECs was observed. Under 0.1% O2, reciprocal effects of ECs and MSCs were similar to those at 5% O2. Meanwhile, upregulation of RUNX2 was canceled, IL-6 decreased, and IL-8 significantly increased. “Protective” effects of MSCs on TNF-α-ECs were less pronounced, manifested as NOS3 downregulation and intracellular NO elevation. Therefore, interaction with ECs at “physiological” hypoxia enhanced pro-regenerative capacities of MSCs including migration and anti-inflammatory modulation of ECs. Under acute hypoxic stress, the stimulating effects of ECs on MSCs and the “protective” potential of MSCs towards TNF-α-ECs were attenuated. Full article
(This article belongs to the Special Issue Advances in the Angiogenic Field)
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15 pages, 2286 KiB  
Article
Heparin–Avastin Complexes Show Enhanced VEGF Binding and Inhibition of VEGF-Mediated Cell Migration
by Divyabharathy Tsiros, Casey E. Sheehy and Matthew A. Nugent
Int. J. Transl. Med. 2021, 1(2), 101-115; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1020008 - 10 Aug 2021
Viewed by 3008
Abstract
Bevacizumab (known by the tradename Avastin) is an antibody that binds VEGF and blocks its binding to VEGF receptors on endothelial cells, and is used to treat cancers and other diseases associated with excessive vascular growth. Our previous findings showed enhanced VEGF binding [...] Read more.
Bevacizumab (known by the tradename Avastin) is an antibody that binds VEGF and blocks its binding to VEGF receptors on endothelial cells, and is used to treat cancers and other diseases associated with excessive vascular growth. Our previous findings showed enhanced VEGF binding to Avastin in the presence of heparin, indicating that colocalizing heparin with Avastin could enhance VEGF inhibitory activity. Thus, the aim of the present study was to determine if conjugating Avastin and heparin to one another would lead to enhanced anti-VEGF activity. Avastin was conjugated to either biotin or streptavidin, and biotin–heparin was used to bring the two molecules into close proximity via biotin–streptavidin binding. Radioligand binding assays with 125 I-VEGF and cell migration assays using human umbilical vein endothelial cells were used to evaluate the impact of heparin on Avastin binding and activity. We found that bringing Avastin and heparin together, either on a surface or through streptavidin conjugation of Avastin, led to increased VEGF binding compared to that with each molecule alone. The heparin-mediated increase in VEGF binding was also noted at acidic pH where Avastin showed decreased VEGF binding. Conditions where Avastin and heparin showed enhanced VEGF binding also showed reduced VEGF-induced migration of human umbilical vein endothelial cells. These findings suggest design principles for a modified Avastin-based inhibitor of angiogenesis. Full article
(This article belongs to the Special Issue Advances in the Angiogenic Field)
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Review

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13 pages, 817 KiB  
Review
A Systematic Review on the Role of Adrenergic Receptors in Angiogenesis Regulation in Health and Disease
by Athanasios Xanthopoulos, Iliana Daskalopoulou, Sofia Frountzi and Evangelia Papadimitriou
Int. J. Transl. Med. 2021, 1(3), 353-365; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1030021 - 30 Nov 2021
Cited by 2 | Viewed by 5948
Abstract
Angiogenesis is essential during development or when tissue restoration and oxygenation is required. Limited or excessive formation of blood vessels is a hallmark of several pathologies, and many angiogenesis-related pathways are being studied to highlight potential targets for effective angiogenesis-stimulating or inhibiting therapeutic [...] Read more.
Angiogenesis is essential during development or when tissue restoration and oxygenation is required. Limited or excessive formation of blood vessels is a hallmark of several pathologies, and many angiogenesis-related pathways are being studied to highlight potential targets for effective angiogenesis-stimulating or inhibiting therapeutic approaches. A few studies point to the adrenergic system as a significant regulator of angiogenesis, directly or indirectly. Functional adrenergic receptors are expressed on endothelial cells and affect their response to the adrenergic system. The latter can also upregulate the release of growth factors by mural cells of the vessel wall, blood cells or cancer cells, thus subsequently affecting endothelial cell functions and angiogenesis. In the present study we summarize up-to-date literature on the known effects of the adrenergic receptors on physiological and pathological angiogenesis. Full article
(This article belongs to the Special Issue Advances in the Angiogenic Field)
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12 pages, 963 KiB  
Review
The Metastatic Capacity of Melanoma Reveals Alternative Pathways of Cancer Dissemination
by Michela Corsini, Cosetta Ravelli, Elisabetta Grillo and Stefania Mitola
Int. J. Transl. Med. 2021, 1(3), 163-174; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1030012 - 01 Oct 2021
Cited by 1 | Viewed by 2741
Abstract
For many years the growth of solid tumors has been associated with their vascularization. The new vessels are needed to deliver oxygen and nutrients within the tumor mass. At the same time, these poorly stabilized vessels act as “Trojan horses” and open a [...] Read more.
For many years the growth of solid tumors has been associated with their vascularization. The new vessels are needed to deliver oxygen and nutrients within the tumor mass. At the same time, these poorly stabilized vessels act as “Trojan horses” and open a way out for cancer cells. More recently, tumors have been identified whose growth appears to be independent of endothelial cell activity. Here we describe the ability of cancer cells to differentiate and reorganize themself in channels similar to blood vessels containing blood flow, overcoming the need for the angiogenic process of tumor vascularization. Together with the new vessels arising both from angiogenic and vasculogenic processes, these vessel-like structures can be exploited by tumor cells as a guide for migration and metastatic dissemination. In addition to classical intravascular dissemination, cancer cells can acquire pericytic features, interact with the endothelial basal lamina and migrate toward vessels or outside of the vessels. As expected, these alternative tumor behaviors assume greater importance if we consider that drugs with anti-angiogenic action directed against endothelial cells or their ligands are currently used in cancer therapy. Full article
(This article belongs to the Special Issue Advances in the Angiogenic Field)
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