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Signal Transduction Pathways Regulated by Vascular Endothelial Growth Factor
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Signal Transduction Pathways Regulated by Vascular Endothelial Growth Factor

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2021) | Viewed by 10449

Special Issue Editor

Prof. Dr. David Della-Morte

E-Mail Website
Guest Editor
1. Department of Systems Medicine, University of Rome Tor Vergata, Via Montpellier 1, 00133 Rome, Italy
2. Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL 33136, USA
Interests: vascular disease; aging; genetics; neurology; epidemiology; basic science; oxidative stress; stroke; atherosclerosis; ischemic preconditioning; diabetes; sarcopenia; nutrition

Special Issue Information

Dear Colleagues,

In the last few decades, among the most controversial and debated transduction signals associated with chronic diseases, such as cancer, cardiovascular disease, neurological disorders, and eye diseases among others, there is the signal transduction regulated by the Vascular Endothelial Growth Factor (VEGF). Since its discovery, VEGF has revolutionized our consideration on all processes of vasculogenesis and angiogenesis during physiological vascular homeostasis underlying tissue growth. VEGF, also known as VEGF-A, is the most well characterized member of the cysteine-knot growth factors family. Hypoxia is a major regulator of VEGF expression via hypoxia inducible factor (HIF). Then, when activated, VEGF displays several activities such as pro-angiogenic function, vascular permeability, and vasodilation. However, as largely demonstrated, these VEGF properties lead to the formation of new blood vessels, which may be structurally abnormal in the case of tumors. Moreover, alternative exon splicing on the vegf gene leads to multiple VEGF isoforms with different pro-angiogenic activities, as well as different single nucleotide polymorphisms (SNPs) in the same gene, which have been associated with a significant variability in the association with chronic diseases in humans. Therapies targeting VEGF and its signal transduction are currently available and research in this field is ongoing. However, it is imperative to understand the complex interactions between VEGF and other signaling pathways regulating the same vascular/tissue processes in order to clearly define the beyond rational and insight of targeting VEGF against chronic diseases. With this aim, original contributions, comprehensive reviews, or perspective articles are more than welcome for this Special Issue.

Prof. Dr. David Della-Morte
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Vascular endothelial growth factor
  • Cardiovascular diseases
  • Cancer
  • Eye diseases
  • Neurological diseases
  • Angiogenesis
  • Genetics
  • Epigenetics
  • Hypoxia
  • Anti-VEGF therapy

Published Papers (2 papers)

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Research

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16 pages, 2585 KiB  
Article
The GAUGAA Motif Is Responsible for the Binding between circSMARCA5 and SRSF1 and Related Downstream Effects on Glioblastoma Multiforme Cell Migration and Angiogenic Potential
by Davide Barbagallo, Angela Caponnetto, Cristina Barbagallo, Rosalia Battaglia, Federica Mirabella, Duilia Brex, Michele Stella, Giuseppe Broggi, Roberto Altieri, Francesco Certo, Rosario Caltabiano, Giuseppe Maria Vincenzo Barbagallo, Carmelina Daniela Anfuso, Gabriella Lupo, Marco Ragusa, Cinzia Di Pietro, Thomas Birkballe Hansen and Michele Purrello
Int. J. Mol. Sci. 2021, 22(4), 1678; https://doi.org/10.3390/ijms22041678 - 07 Feb 2021
Cited by 44 | Viewed by 3332
Abstract
Circular RNAs (circRNAs) are a large class of RNAs with regulatory functions within cells. We recently showed that circSMARCA5 is a tumor suppressor in glioblastoma multiforme (GBM) and acts as a decoy for Serine and Arginine Rich Splicing Factor 1 (SRSF1) through six [...] Read more.
Circular RNAs (circRNAs) are a large class of RNAs with regulatory functions within cells. We recently showed that circSMARCA5 is a tumor suppressor in glioblastoma multiforme (GBM) and acts as a decoy for Serine and Arginine Rich Splicing Factor 1 (SRSF1) through six predicted binding sites (BSs). Here we characterized RNA motifs functionally involved in the interaction between circSMARCA5 and SRSF1. Three different circSMARCA5 molecules (Mut1, Mut2, Mut3), each mutated in two predicted SRSF1 BSs at once, were obtained through PCR-based replacement of wild-type (WT) BS sequences and cloned in three independent pcDNA3 vectors. Mut1 significantly decreased its capability to interact with SRSF1 as compared to WT, based on the RNA immunoprecipitation assay. In silico analysis through the “Find Individual Motif Occurrences” (FIMO) algorithm showed GAUGAA as an experimentally validated SRSF1 binding motif significantly overrepresented within both predicted SRSF1 BSs mutated in Mut1 (q-value = 0.0011). U87MG and CAS-1, transfected with Mut1, significantly increased their migration with respect to controls transfected with WT, as revealed by the cell exclusion zone assay. Immortalized human brain microvascular endothelial cells (IM-HBMEC) exposed to conditioned medium (CM) harvested from U87MG and CAS-1 transfected with Mut1 significantly sprouted more than those treated with CM harvested from U87MG and CAS-1 transfected with WT, as shown by the tube formation assay. qRT-PCR showed that the intracellular pro- to anti-angiogenic Vascular Endothelial Growth Factor A (VEGFA) mRNA isoform ratio and the amount of total VEGFA mRNA secreted in CM significantly increased in Mut1-transfected CAS-1 as compared to controls transfected with WT. Our data suggest that GAUGAA is the RNA motif responsible for the interaction between circSMARCA5 and SRSF1 as well as for the circSMARCA5-mediated control of GBM cell migration and angiogenic potential. Full article
(This article belongs to the Special Issue Signal Transduction Pathways Regulated by Vascular Endothelial Growth Factor)
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Review

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17 pages, 1672 KiB  
Review
Vascular Endothelial Growth Factor, a Key Modulator of the Anti-Tumor Immune Response
by Mannon Geindreau, François Ghiringhelli and Mélanie Bruchard
Int. J. Mol. Sci. 2021, 22(9), 4871; https://doi.org/10.3390/ijms22094871 - 04 May 2021
Cited by 38 | Viewed by 6362
Abstract
During tumor growth, angiogenesis is required to ensure oxygen and nutrient transport to the tumor. Vascular endothelial growth factor (VEGF) is the major inducer of angiogenesis and appears to be a key modulator of the anti-tumor immune response. Indeed, VEGF modulates innate and [...] Read more.
During tumor growth, angiogenesis is required to ensure oxygen and nutrient transport to the tumor. Vascular endothelial growth factor (VEGF) is the major inducer of angiogenesis and appears to be a key modulator of the anti-tumor immune response. Indeed, VEGF modulates innate and adaptive immune responses through direct interactions and indirectly by modulating protein expressions on endothelial cells or vascular permeability. The inhibition of the VEGF signaling pathway is clinically approved for the treatment of several cancers. Therapies targeting VEGF can modulate the tumor vasculature and the immune response. In this review, we discuss the roles of VEGF in the anti-tumor immune response. In addition, we summarize therapeutic strategies based on its inhibition, and their clinical approval. Full article
(This article belongs to the Special Issue Signal Transduction Pathways Regulated by Vascular Endothelial Growth Factor)
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