Special Issue "Advances in the Angiogenic Field"

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 and Collections 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
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

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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 (2 papers)

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Research

Article
Crosstalk of Endothelial and Mesenchymal Stromal Cells under Tissue-Related O2
Int. J. Transl. Med. 2021, 1(2), 116-136; https://0-doi-org.brum.beds.ac.uk/10.3390/ijtm1020009 - 07 Sep 2021
Viewed by 294
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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Article
Heparin–Avastin Complexes Show Enhanced VEGF Binding and Inhibition of VEGF-Mediated Cell Migration
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 328
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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