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Biomedicines
Special Issues
Angiogenesis and Anti-angiogenesis in Health and Diseases 2.0
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Angiogenesis and Anti-angiogenesis in Health and Diseases 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 15063

Special Issue Editor

Dr. Elmina Mammadova-Bach

E-Mail Website
Guest Editor
Walther-Straub-Institute for Pharmacology and Toxicology, Ludwig-Maximilian-University, Munich, Germany
Interests: cancer; metastasis; tumor microenvironment; circulating blood cells; coagulation; platelets; cancer-associated thrombosis; angiogenesis; lymphangiogenesis; inflammatory ecosystem of tumors; mechanisms of resistance to the anti-cancer therapies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolites, nutrients, oxygen and chemical mediators are transported through the blood vessels to maintain and regulate essential physiological functions including organ homeostasis, immune system, body temperature and growth. Vessel formation, angiogenesis is one of the fundamental biological processes involved in embryonic development and also in the growth and metastasis of tumors. Angiogenic switch is an important event during tumor progression where the balance between pro and antiangiogenic factors slope towards a proangiogenic outcome, leading to the transition from avascularized neoplasia to a vascularized tumor. This process of neovascularization was considered a key factor influencing cancer growth. However, several pieces of evidence indicate alternative methods by which blood vessels may influence tumor growth and metastasis, such as vessel cooption, vascular mimicry and intussusceptive angiogenesis. Tumor vessels often appeared abnormal in shape and function, and they are more loosely connected with surrounding cells, such as pericytes and smooth muscle vascular cells, influencing drug delivery. Therefore, preclinical and clinical studies have focused on the role of mural cells, stabilizing the tumor vasculature through various signaling pathways, which influence many hallmarks of cancer, including immune modulation, cell survival and death. However, both defective vasculature and excessive ECM generation and pericyte coverage represent a physical barrier for effective drug delivery, leading to the resistance to the anti-tumor therapies. The efficacy of therapies is also modulated by circulating blood cells, such as monocytes, neutrophils and platelets, which depending on the pathological situation may maintain the integrity of vessels or induce permeability, and creating regenerative, prothrombotic and or proinflammatory environment. Angiogenesis is not limited to cancer; it is also occurring under other pathological conditions, such as diabetic retinopathy, ischemic stroke, myelofibrosis, sickle cell diseases, rheumatoid arthritis, vasculitis and atherogenesis. Current efforts aim to advance research toward the discovery of new molecular targets, gene profiling, resistance mechanisms, and diagnostic and prognostic markers to overcome disease progression by improving the therapeutic options.

Dr. Elmina Mammadova-Bach
Guest Editor

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • cancer
  • tumor microenvironment
  • metastatic niches
  • angiogenesis
  • coagulation
  • blood clotting
  • vascular integrity
  • inflammation
  • thrombo-inflammation
  • vasculogenesis
  • lympangiogenesis
  • diabetic retinopathy
  • wound healing
  • immune cells
  • neutrophils and NETs
  • cancer and angiogenic dormancy
  • bone marrow ecosystem
  • fibrosis
  • myelofibrosis
  • synovial inflammation
  • vasculitis
  • resistance to the anti-angiogenic and anti-cancer therapies

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Published Papers (4 papers)

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Research

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15 pages, 1781 KiB  
Article
Uptake-Dependent and -Independent Effects of Fibroblasts-Derived Extracellular Vesicles on Bone Marrow Endothelial Cells from Patients with Multiple Myeloma: Therapeutic and Clinical Implications
by Aurelia Lamanuzzi, Ilaria Saltarella, Antonia Reale, Assunta Melaccio, Antonio Giovanni Solimando, Concetta Altamura, Grazia Tamma, Clelia Tiziana Storlazzi, Doron Tolomeo, Vanessa Desantis, Maria Addolorata Mariggiò, Jean-François Desaphy, Andrew Spencer, Angelo Vacca, Benedetta Apollonio and Maria Antonia Frassanito
Biomedicines 2023, 11(5), 1400; https://doi.org/10.3390/biomedicines11051400 - 8 May 2023
Viewed by 1959
Abstract
Extracellular vesicles (EVs) have emerged as important players in cell-to-cell communication within the bone marrow (BM) of multiple myeloma (MM) patients, where they mediate several tumor-associated processes. Here, we investigate the contribution of fibroblasts-derived EVs (FBEVs) in supporting BM angiogenesis. We demonstrate that [...] Read more.
Extracellular vesicles (EVs) have emerged as important players in cell-to-cell communication within the bone marrow (BM) of multiple myeloma (MM) patients, where they mediate several tumor-associated processes. Here, we investigate the contribution of fibroblasts-derived EVs (FBEVs) in supporting BM angiogenesis. We demonstrate that FBEVs’ cargo contains several angiogenic cytokines (i.e., VEGF, HGF, and ANG-1) that promote an early over-angiogenic effect independent from EVs uptake. Interestingly, co-culture of endothelial cells from MM patients (MMECs) with FBEVs for 1 or 6 h activates the VEGF/VEGFR2, HGF/HGFR, and ANG-1/Tie2 axis, as well as the mTORC2 and Wnt/β-catenin pathways, suggesting that the early over-angiogenic effect is a cytokine-mediated process. FBEVs internalization occurs after longer exposure of MMECs to FBEVs (24 h) and induces a late over-angiogenic effect by increasing MMECs migration, chemotaxis, metalloproteases release, and capillarogenesis. FBEVs uptake activates mTORC1, MAPK, SRC, and STAT pathways that promote the release of pro-angiogenic cytokines, further supporting the pro-angiogenic milieu. Overall, our results demonstrate that FBEVs foster MM angiogenesis through dual time-related uptake-independent and uptake-dependent mechanisms that activate different intracellular pathways and transcriptional programs, providing the rationale for designing novel anti-angiogenic strategies. Full article
(This article belongs to the Special Issue Angiogenesis and Anti-angiogenesis in Health and Diseases 2.0)
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17 pages, 2376 KiB  
Article
Minimal Collagen-Binding Epitope of Glycoprotein VI in Human and Mouse Platelets
by Chao Han, Pengxuan Ren, Medina Mamtimin, Linus Kruk, Edita Sarukhanyan, Chenyu Li, Hans-Joachim Anders, Thomas Dandekar, Irena Krueger, Margitta Elvers, Silvia Goebel, Kristin Adler, Götz Münch, Thomas Gudermann, Attila Braun and Elmina Mammadova-Bach
Biomedicines 2023, 11(2), 423; https://doi.org/10.3390/biomedicines11020423 - 1 Feb 2023
Cited by 1 | Viewed by 2738
Abstract
Glycoprotein VI (GPVI) is a platelet-specific receptor for collagen and fibrin, regulating important platelet functions such as platelet adhesion and thrombus growth. Although the blockade of GPVI function is widely recognized as a potent anti-thrombotic approach, there are limited studies focused on site-specific [...] Read more.
Glycoprotein VI (GPVI) is a platelet-specific receptor for collagen and fibrin, regulating important platelet functions such as platelet adhesion and thrombus growth. Although the blockade of GPVI function is widely recognized as a potent anti-thrombotic approach, there are limited studies focused on site-specific targeting of GPVI. Using computational modeling and bioinformatics, we analyzed collagen- and CRP-binding surfaces of GPVI monomers and dimers, and compared the interacting surfaces with other mammalian GPVI isoforms. We could predict a minimal collagen-binding epitope of GPVI dimer and designed an EA-20 antibody that recognizes a linear epitope of this surface. Using platelets and whole blood samples donated from wild-type and humanized GPVI transgenic mice and also humans, our experimental results show that the EA-20 antibody inhibits platelet adhesion and aggregation in response to collagen and CRP, but not to fibrin. The EA-20 antibody also prevents thrombus formation in whole blood, on the collagen-coated surface, in arterial flow conditions. We also show that EA-20 does not influence GPVI clustering or receptor shedding. Therefore, we propose that blockade of this minimal collagen-binding epitope of GPVI with the EA-20 antibody could represent a new anti-thrombotic approach by inhibiting specific interactions between GPVI and the collagen matrix. Full article
(This article belongs to the Special Issue Angiogenesis and Anti-angiogenesis in Health and Diseases 2.0)
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19 pages, 3799 KiB  
Article
TGF-Beta Modulates the Integrity of the Blood Brain Barrier In Vitro, and Is Associated with Metabolic Alterations in Pericytes
by Leonie Schumacher, Rédouane Slimani, Laimdota Zizmare, Jakob Ehlers, Felix Kleine Borgmann, Julia C. Fitzgerald, Petra Fallier-Becker, Anja Beckmann, Alexander Grißmer, Carola Meier, Ali El-Ayoubi, Kavi Devraj, Michel Mittelbronn, Christoph Trautwein and Ulrike Naumann
Biomedicines 2023, 11(1), 214; https://doi.org/10.3390/biomedicines11010214 - 14 Jan 2023
Cited by 6 | Viewed by 3613
Abstract
The blood–brain barrier (BBB) is a selectively permeable boundary that separates the circulating blood from the extracellular fluid of the brain and is an essential component for brain homeostasis. In glioblastoma (GBM), the BBB of peritumoral vessels is often disrupted. Pericytes, being important [...] Read more.
The blood–brain barrier (BBB) is a selectively permeable boundary that separates the circulating blood from the extracellular fluid of the brain and is an essential component for brain homeostasis. In glioblastoma (GBM), the BBB of peritumoral vessels is often disrupted. Pericytes, being important to maintaining BBB integrity, can be functionally modified by GBM cells which induce proliferation and cell motility via the TGF-β-mediated induction of central epithelial to mesenchymal transition (EMT) factors. We demonstrate that pericytes strengthen the integrity of the BBB in primary endothelial cell/pericyte co-cultures as an in vitro BBB model, using TEER measurement of the barrier integrity. In contrast, this effect was abrogated by TGF-β or conditioned medium from TGF-β secreting GBM cells, leading to the disruption of a so far intact and tight BBB. TGF-β notably changed the metabolic behavior of pericytes, by shutting down the TCA cycle, driving energy generation from oxidative phosphorylation towards glycolysis, and by modulating pathways that are necessary for the biosynthesis of molecules used for proliferation and cell division. Combined metabolomic and transcriptomic analyses further underscored that the observed functional and metabolic changes of TGF-β-treated pericytes are closely connected with their role as important supporting cells during angiogenic processes. Full article
(This article belongs to the Special Issue Angiogenesis and Anti-angiogenesis in Health and Diseases 2.0)
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Review

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29 pages, 3721 KiB  
Review
Angiogenesis and Tissue Repair Depend on Platelet Dosing and Bioformulation Strategies Following Orthobiological Platelet-Rich Plasma Procedures: A Narrative Review
by Peter A. Everts, José Fábio Lana, Kentaro Onishi, Don Buford, Jeffrey Peng, Ansar Mahmood, Lucas F. Fonseca, Andre van Zundert and Luga Podesta
Biomedicines 2023, 11(7), 1922; https://doi.org/10.3390/biomedicines11071922 - 6 Jul 2023
Cited by 19 | Viewed by 6193
Abstract
Angiogenesis is the formation of new blood vessel from existing vessels and is a critical first step in tissue repair following chronic disturbances in healing and degenerative tissues. Chronic pathoanatomic tissues are characterized by a high number of inflammatory cells; an overexpression of [...] Read more.
Angiogenesis is the formation of new blood vessel from existing vessels and is a critical first step in tissue repair following chronic disturbances in healing and degenerative tissues. Chronic pathoanatomic tissues are characterized by a high number of inflammatory cells; an overexpression of inflammatory mediators; such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1); the presence of mast cells, T cells, reactive oxygen species, and matrix metalloproteinases; and a decreased angiogenic capacity. Multiple studies have demonstrated that autologous orthobiological cellular preparations (e.g., platelet-rich plasma (PRP)) improve tissue repair and regenerate tissues. There are many PRP devices on the market. Unfortunately, they differ greatly in platelet numbers, cellular composition, and bioformulation. PRP is a platelet concentrate consisting of a high concentration of platelets, with or without certain leukocytes, platelet-derived growth factors (PGFs), cytokines, molecules, and signaling cells. Several PRP products have immunomodulatory capacities that can influence resident cells in a diseased microenvironment, inducing tissue repair or regeneration. Generally, PRP is a blood-derived product, regardless of its platelet number and bioformulation, and the literature indicates both positive and negative patient treatment outcomes. Strangely, the literature does not designate specific PRP preparation qualifications that can potentially contribute to tissue repair. Moreover, the literature scarcely addresses the impact of platelets and leukocytes in PRP on (neo)angiogenesis, other than a general one-size-fits-all statement that “PRP has angiogenic capabilities”. Here, we review the cellular composition of all PRP constituents, including leukocytes, and describe the importance of platelet dosing and bioformulation strategies in orthobiological applications to initiate angiogenic pathways that re-establish microvasculature networks, facilitating the supply of oxygen and nutrients to impaired tissues. Full article
(This article belongs to the Special Issue Angiogenesis and Anti-angiogenesis in Health and Diseases 2.0)
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