Molecular and Cellular Biology of Angiogenesis

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 495

Special Issue Editor


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Guest Editor
Department of Surgery, Vascular Division—Miller School of Medicine, University of Miami, Miami, FL 33136, USA
Interests: peripheral arterial disease; neovascularization; arteriogenesis; inflammation; ischemia

Special Issue Information

Dear Colleagues,

Angiogenesis is the physiological process through which new blood vessels form from pre-existing vessels. This hypoxia-mediated sprouting of new capillaries is crucial for neovascularization, development, and wound healing. It also plays a significant role in pathological conditions such as cancer, diabetic retinopathy, and rheumatoid arthritis. Understanding the molecular and cellular mechanisms underlying angiogenesis is essential for developing targeted therapies for these diseases. There are critical, well-known molecular players in angiogenesis, which include (but are not limited to) vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), angiopoietins (Ang1 and Ang2), and matrix metalloproteinases (MMPs), that have been studied in different vascular conditions. Moreover, there are essential cellular mechanisms in angiogenesis, such as endothelial cell proliferation, differentiation of tip and stalk cells, blood flow regulation/shear stress, and lumen formation. These mechanisms might be associated with hypoxia-inducible factors (HIFs) and integrins, which are angiogenic regulators. By investigating these molecular and cellular mechanisms, scientists aim to develop targeted therapies that can promote or inhibit angiogenesis, depending on the clinical context. Understanding the balance between pro-angiogenic and anti-angiogenic signals is crucial for managing physiological and pathological blood vessel formation.

In light of the above background, this Special Issue titled “Molecular and Cellular Biology of Angiogenesis" will feature studies that enrich the knowledge and explore therapeutical approaches that promote angiogenesis. 

Dr. Roberta Marques Lassance-Soares
Guest Editor

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Keywords

  • neovascularization
  • endothelial proliferation
  • vascular growth

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Published Papers (1 paper)

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Research

16 pages, 4385 KiB  
Article
Adeno-Associated Virus-Engineered Umbilical Cord-Derived Mesenchymal Stromal Cells Overexpressing Human sFlt-1 for Anti-Angiogenesis
by Ewa Yee-Wa Choy, Chee-Onn Leong, Soon-Keng Cheong, Khong-Lek Then and Kong-Yong Then
Life 2025, 15(5), 728; https://doi.org/10.3390/life15050728 (registering DOI) - 30 Apr 2025
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Abstract
Purpose. Genetic engineering of mesenchymal stromal cells (MSCs) using viral vectors has emerged as a promising approach to enhance the efficacy of anti-angiogenic gene therapies. Umbilical cord-derived MSCs are an attractive cell source due to their easy accessibility and potential for genetic modification. [...] Read more.
Purpose. Genetic engineering of mesenchymal stromal cells (MSCs) using viral vectors has emerged as a promising approach to enhance the efficacy of anti-angiogenic gene therapies. Umbilical cord-derived MSCs are an attractive cell source due to their easy accessibility and potential for genetic modification. Adeno-associated viruses (AAVs) have been utilized in clinical settings to deliver therapeutic genes due to its characteristic of transient integration into the genome. In this study, we investigated the efficacy of using recombinant AAV-engineered umbilical cord-derived MSCs overexpressing anti-angiogenic factor, hsFlt-1 (MSCs.hsFlt1). Methods. The plasmid containing the hsFlt-1 gene was cloned into the AAV2 target backbone and validated using Sanger sequencing. The transduction process was studied to determine the optimal conditions, including the effect of MOI, media serum percentage, and attachment of MSCs, to achieve higher transduction efficiency. The functionality of MSCs.hsFtl1 was analyzed using qPCR, ELISA, and tube formation assays. Results. MSCs.hsFtl1 transduced at an MOI of 1 × 106 demonstrated high transduction efficiency and exhibited robust gene and protein expression of hsFlt-1. The results revealed significant inhibition of growth in human umbilical vein endothelial cells (HUVECs) using a remarkably low dose of MSCs.hsFlt1 at 12.3 ng/mL. This observed anti-angiogenic effect was comparable to the clinically used Bevacizumab. Conclusions. The anti-angiogenic potential of MSCs.hsFlt1 effectively demonstrated in this study suggests their promising utility for targeted anti-angiogenic gene therapy approaches. Full article
(This article belongs to the Special Issue Molecular and Cellular Biology of Angiogenesis)
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