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Biomedicines
Special Issues
Adult Stem Cells and Endothelial Progenitor Cells in Diseases
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Adult Stem Cells and Endothelial Progenitor Cells in Diseases

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

Deadline for manuscript submissions: closed (31 July 2023) | Viewed by 3572

Special Issue Editor

Dr. Jolanta Weaver

E-Mail Website
Guest Editor
Institute of Cellular Medicine, Newcastle University, Newcastle, UK
Interests: cardiovascular disease; diabetes mellitus; vascular stem cells; endothelial progenitor cells; repurposing metformin for CVD; risk factors for CVD; in-vitro models of CVD
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endothelial progenitor cells (EPCs) represent a subpopulation of mononuclear cells (MNCs) that are recruited to replace senescent/injured vascular endothelial cells, reconstruct injured vessels, and restore local blood flow upon an ischemic insult. Furthermore, EPCs play a crucial role during the angiogenic switch that supports vascularization, growth, and metastasis in solid tumours.

As proposed in a recent consensus statement, two distinct and well-defined EPC subtypes may emerge from cultured mononuclear cells, which differ in their ontology and reparative mechanisms. These EPC subtypes include: myeloid angiogenic cells (MACs), also termed circulating angiogenic cells (CACs), pro-angiogenic hematopoietic cells (PAC), pro-angiogenic circulating hematopoietic stem/progenitor cells (pro-CHSPCs or pro-CPCs), or “early” EPCs; and endothelial colony-forming cells (ECFCs), also known as outgrowth endothelial cells (OECs) or “late” EPCs. EPCs may support neovascularization of ischemic tissues through the paracrine release of growth factors and cytokines, including vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), stromal cell-derived factor-1a (SDF-1a) or by physically incorporating within nascent neovessels.

Autologous MACs were probed in no less than 150 registered interventional clinical trials to induce therapeutic angiogenesis in multiple cardiovascular disorders, including myocardial infarction, critical limb ischemia, leg ulcer/gangrene, peripheral artery disease, hypertension, diabetic micro-vasculopathy, and stroke. Moreover, interfering with EPC recruitment to tumour sites is regarded as an alternative strategy to interfere with tumour growth and metastasis in cancer patients.

New research results are also emerging on the role of microRNAs in the pathways related to EPCs.

I am therefore pleased to invite all of you to participate in this Special Issue by presenting your most recent research or ideas about the definition, identity, pathophysiology, and therapeutic application of EPCs. Original research articles and comprehensive review papers are all welcome.

Dr. Jolanta Weaver
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.

Published Papers (3 papers)

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Research

16 pages, 2832 KiB  
Article
Upregulation of Anti-Angiogenic miR-106b-3p Correlates Negatively with IGF-1 and Vascular Health Parameters in a Model of Subclinical Cardiovascular Disease: Study with Metformin Therapy
by Sherin Bakhashab, Josie O’Neill, Rosie Barber, Catherine Arden and Jolanta U. Weaver
Biomedicines 2024, 12(1), 171; https://doi.org/10.3390/biomedicines12010171 - 12 Jan 2024
Viewed by 795
Abstract
Well-controlled type 1 diabetes mellitus (T1DM) is regarded as a model of subclinical cardiovascular disease (CVD), characterized by inflammation and adverse vascular health. However, the underlying mechanisms are not fully understood. We investigated insulin-like growth factor-1 (IGF-1) and IGF-binding protein-3 (IGFBP-3) levels, their [...] Read more.
Well-controlled type 1 diabetes mellitus (T1DM) is regarded as a model of subclinical cardiovascular disease (CVD), characterized by inflammation and adverse vascular health. However, the underlying mechanisms are not fully understood. We investigated insulin-like growth factor-1 (IGF-1) and IGF-binding protein-3 (IGFBP-3) levels, their correlation to miR-106b-3p expression in a subclinical CVD model, and the cardioprotective effect of metformin. A total of 20 controls and 29 well-controlled T1DM subjects were studied. Plasma IGF-1, IGFBP-3 levels, and miR-106b-3p expression in colony-forming unit-Hills were analyzed and compared with vascular markers. miR-106b-3p was upregulated in T1DM (p < 0.05) and negatively correlated with pro-angiogenic markers CD34+/100-lymphocytes (p < 0.05) and IGF-1 (p < 0.05). IGF-1 was downregulated in T1DM (p < 0.01), which was associated with increased inflammatory markers TNF-α, CRP, and IL-10 and reduced CD34+/100-lymphocytes. IGFBP-3 had no significant results. Metformin had no effect on IGF-1 but significantly reduced miR-106b-3p (p < 0.0001). An Ingenuity Pathway analysis predicted miR-106b-3p to inhibit PDGFA, PIK3CG, GDNF, and ADAMTS13, which activated CVD. Metformin was predicted to be cardioprotective by inhibiting miR-106b-3p. In conclusion: Subclinical CVD is characterized by a cardio-adverse profile of low IGF-1 and upregulated miR-106b-3p. We demonstrated that the cardioprotective effect of metformin may be via downregulation of upregulated miR-106b-3p and its effect on downstream targets. Full article
(This article belongs to the Special Issue Adult Stem Cells and Endothelial Progenitor Cells in Diseases)
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13 pages, 1608 KiB  
Article
Development of Personalized Thrombogenesis and Thrombin Generation Assays to Assess Endothelial Dysfunction in Cardiovascular Diseases
by Monica Bacci, Assunta Cancellara, Roberta Ciceri, Erica Romualdi, Valentina Pessi, Fabio Tumminello, Martina Fantuzzi, Marco Paolo Donadini, Corrado Lodigiani, Silvia Della Bella, Francesca Calcaterra and Domenico Mavilio
Biomedicines 2023, 11(6), 1669; https://doi.org/10.3390/biomedicines11061669 - 8 Jun 2023
Cited by 1 | Viewed by 1104
Abstract
The study of endothelial dysfunction (ED) is crucial to identify the pathogenetic mechanism(s) and provide indications for patient management in cardiovascular diseases. It is currently hindered by the limited availability of patient-specific primary endothelial cells (ECs). Endothelial colony-forming cells (ECFCs) represent an optimal [...] Read more.
The study of endothelial dysfunction (ED) is crucial to identify the pathogenetic mechanism(s) and provide indications for patient management in cardiovascular diseases. It is currently hindered by the limited availability of patient-specific primary endothelial cells (ECs). Endothelial colony-forming cells (ECFCs) represent an optimal non-invasive tool to overcome this issue. Therefore, we investigated the use of ECFCs as a substrate in thrombogenesis and thrombin generation assay (TGA) to assess ED. Both assays were set up on human umbilical vein endothelial cells (HUVECs) and then tested on ECFCs obtained from healthy donors. To prove the ability of the assays to detect endothelial activation, ECs stimulated with TNFα were compared with unstimulated ECs. EC activation was confirmed by the upregulation of VCAM-1 and Tissue Factor expression. Both assays discriminated between unstimulated and activated HUVECs and ECFCs, as significantly higher platelet deposition and fibrin formation in thrombogenesis assay, and thrombin generation in TGA, were observed when TNFα-activated ECs were used as a substrate. The amount of fibrin and thrombin measured in the two assays were directly correlated. Our results support the combined use of a thrombogenesis assay and TGA performed on patient-derived ECFCs to provide a personalized global assessment of ED relevant to the patient’s hemostatic profile. Full article
(This article belongs to the Special Issue Adult Stem Cells and Endothelial Progenitor Cells in Diseases)
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20 pages, 5604 KiB  
Article
Augmenting the Angiogenic Profile and Functionality of Cord Blood Endothelial Colony-Forming Cells by Indirect Priming with Bone-Marrow-Derived Mesenchymal Stromal Cells
by Ashutosh Bansal, Archna Singh, Tapas Chandra Nag, Devyani Sharma, Bhavuk Garg, Neerja Bhatla, Saumitra Dey Choudhury and Lakshmy Ramakrishnan
Biomedicines 2023, 11(5), 1372; https://doi.org/10.3390/biomedicines11051372 - 5 May 2023
Viewed by 1241
Abstract
Cellular therapy has shown promise as a strategy for the functional restoration of ischemic tissues through promoting vasculogenesis. Therapy with endothelial progenitor cells (EPCs) has shown encouraging results in preclinical studies, but the limited engraftment, inefficient migration, and poor survival of patrolling endothelial [...] Read more.
Cellular therapy has shown promise as a strategy for the functional restoration of ischemic tissues through promoting vasculogenesis. Therapy with endothelial progenitor cells (EPCs) has shown encouraging results in preclinical studies, but the limited engraftment, inefficient migration, and poor survival of patrolling endothelial progenitor cells at the injured site hinder its clinical utilization. These limitations can, to some extent, be overcome by co-culturing EPCs with mesenchymal stem cells (MSCs). Studies on the improvement in functional capacity of late EPCs, also referred to as endothelial colony-forming cells (ECFCs), when cultured with MSCs have mostly focused on the angiogenic potential, although migration, adhesion, and proliferation potential also determine effective physiological vasculogenesis. Alteration in angiogenic proteins with co-culturing has also not been studied. We co-cultured ECFCs with MSCs via both direct and indirect means, and studied the impact of the resultant contact-mediated and paracrine-mediated impact of MSCs over ECFCs, respectively, on the functional aspects and the angiogenic protein signature of ECFCs. Both directly and indirectly primed ECFCs significantly restored the adhesion and vasculogenic potential of impaired ECFCs, whereas indirectly primed ECFCs showed better proliferation and migratory potential than directly primed ECFCs. Additionally, indirectly primed ECFCs, in their angiogenesis proteomic signature, showed alleviated inflammation, along with the balanced expression of various growth factors and regulators of angiogenesis. Full article
(This article belongs to the Special Issue Adult Stem Cells and Endothelial Progenitor Cells in Diseases)
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