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IJMS
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Angiogenic and Pathological Performance of Vascular Endothelial Cells
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Angiogenic and Pathological Performance of Vascular Endothelial Cells

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 December 2023) | Viewed by 6089

Special Issue Editors

Dr. Jun Zhang

E-Mail
Guest Editor
Texas Tech University Health Sciences Center El Paso, El Paso, TX 79409 801, USA
Interests: angiogenesis; tumorigenesis; molecular genetics; molecular biology; biochemistry
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Daniele Rigamonti

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Guest Editor
Department of Neurosurgery, Johns Hopkins University, Baltimore, MD 21218, USA
Interests: neurosurgery; neurosurgeon
Dr. Mary Wallingford

E-Mail Website
Guest Editor
Mother Infant Research Institute, Tufts Medical Center, Boston, MA 02111, USA
Interests: vascular biology of pregnancy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The endothelium is a single layer of squamous endothelial cells that lines the interior surface of blood vessels and lymphatic vessels. The endothelium forms an interface between circulating blood or lymph in the lumen and the rest of the vessel wall. Endothelial cells form the barrier between vessels and tissue and control the flow of substances and fluids into and out of a tissue.

Endothelial cells that are in direct contact with blood are called vascular endothelial cells, whereas those in direct contact with lymph are known as lymphatic endothelial cells. Vascular endothelial cells line the entire circulatory system, from the heart to the smallest capillaries.

These cells have unique functions that include fluid filtration, such as in the glomerulus of the kidney, blood vessel tone, hemostasis, neutrophil recruitment and hormone trafficking. The endothelium of the interior surfaces of the heart chambers is called the endocardium. An impaired function can lead to serious health issues throughout the body.

We are soliciting contributions from experts in the vascular endothelial cell (EC) research field. This issue will focus on the angiogenic and pathological performance of vascular/microvascular ECs, covering activation, proliferation, migration, invasion, tube formation, the clonal expansion of ECs and cell junctions, maintenance and the malformations of vasculatures and the blood–brain barrier (BBB). Papers published in IJMS (International Journal of Molecular Sciences) are welcome in order to include results at both the cellular and molecular level. 

Dr. Jun Zhang
Prof. Dr. Daniele Rigamonti
Dr. Mary C. Wallingford
Guest Editors

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

  • angiogenesis
  • endothelial cells (ECs)
  • vascular
  • microvascular
  • angiogenic performance
  • activation
  • proliferation
  • migration
  • invasion
  • tube formation
  • clonal expansion
  • maintenance
  • blood–brain barrier (BBB)
  • malformations
  • cell junctions

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Published Papers (3 papers)

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16 pages, 2503 KiB  
Article
Endothelial Cell Response to Combined Photon or Proton Irradiation with Doxorubicin
by Teresa Bernardo, Anna Kuntze, Diana Klein, Feline Heinzelmann, Beate Timmermann and Cläre von Neubeck
Int. J. Mol. Sci. 2023, 24(16), 12833; https://doi.org/10.3390/ijms241612833 - 16 Aug 2023
Cited by 1 | Viewed by 1474
Abstract
Surgery, radiotherapy, and chemotherapy are essential treatment modalities to target cancer cells, but they frequently cause damage to the normal tissue, potentially leading to side effects. As proton beam radiotherapy (PBT) can precisely spare normal tissue, this therapeutic option is of increasing importance [...] Read more.
Surgery, radiotherapy, and chemotherapy are essential treatment modalities to target cancer cells, but they frequently cause damage to the normal tissue, potentially leading to side effects. As proton beam radiotherapy (PBT) can precisely spare normal tissue, this therapeutic option is of increasing importance regarding (neo-)adjuvant and definitive anti-cancer therapies. Akin to photon-based radiotherapy, PBT is often combined with systemic treatment, such as doxorubicin (Dox). This study compares the cellular response of human microvascular endothelial cells (HMEC-1) following irradiation with photons (X) or protons (H) alone and also in combination with different sequences of Dox. The cellular survival, cell cycle, apoptosis, proliferation, viability, morphology, and migration were all investigated. Dox monotreatment had minor effects on all endpoints. Both radiation qualities alone and in combination with longer Dox schedules significantly reduced clonogenic survival and proliferation, increased the apoptotic cell fraction, induced a longer G2/M cell cycle arrest, and altered the cell morphology towards endothelial-to-mesenchymal-transition (EndoMT) processes. Radiation quality effects were seen for metabolic viability, proliferation, and motility of HMEC-1 cells. Additive effects were found for longer Dox schedules. Overall, similar effects were found for H/H-Dox and X/X-Dox. Significant alterations between the radiation qualities indicate different but not worse endothelial cell damage by H/H-Dox. Full article
(This article belongs to the Special Issue Angiogenic and Pathological Performance of Vascular Endothelial Cells)
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18 pages, 18838 KiB  
Article
Resveratrol Reverses Endothelial Colony-Forming Cell Dysfunction in Adulthood in a Rat Model of Intrauterine Growth Restriction
by Estelle Guillot, Anna Lemay, Manon Allouche, Sara Vitorino Silva, Hanna Coppola, Florence Sabatier, Françoise Dignat-George, Alexandre Sarre, Anne-Christine Peyter, Stéphanie Simoncini and Catherine Yzydorczyk
Int. J. Mol. Sci. 2023, 24(11), 9747; https://doi.org/10.3390/ijms24119747 - 5 Jun 2023
Cited by 4 | Viewed by 1567
Abstract
Individuals born after intrauterine growth restriction (IUGR) are at risk of developing cardiovascular diseases (CVDs). Endothelial dysfunction plays a role in the pathogenesis of CVDs; and endothelial colony-forming cells (ECFCs) have been identified as key factors in endothelial repair. In a rat model [...] Read more.
Individuals born after intrauterine growth restriction (IUGR) are at risk of developing cardiovascular diseases (CVDs). Endothelial dysfunction plays a role in the pathogenesis of CVDs; and endothelial colony-forming cells (ECFCs) have been identified as key factors in endothelial repair. In a rat model of IUGR induced by a maternal low-protein diet, we observed an altered functionality of ECFCs in 6-month-old males, which was associated with arterial hypertension related to oxidative stress and stress-induced premature senescence (SIPS). Resveratrol (R), a polyphenol compound, was found to improve cardiovascular function. In this study, we investigated whether resveratrol could reverse ECFC dysfunctions in the IUGR group. ECFCs were isolated from IUGR and control (CTRL) males and were treated with R (1 μM) or dimethylsulfoxide (DMSO) for 48 h. In the IUGR-ECFCs, R increased proliferation (5′-bromo-2′-deoxyuridine (BrdU) incorporation, p < 0.001) and improved capillary-like outgrowth sprout formation (in Matrigel), nitric oxide (NO) production (fluorescent dye, p < 0.01), and endothelial nitric oxide synthase (eNOS) expression (immunofluorescence, p < 0.001). In addition, R decreased oxidative stress with reduced superoxide anion production (fluorescent dye, p < 0.001); increased Cu/Zn superoxide dismutase expression (Western blot, p < 0.05); and reversed SIPS with decreased beta-galactosidase activity (p < 0.001), and decreased p16ink4a (p < 0.05) and increased Sirtuin-1 (p < 0.05) expressions (Western blot). No effects of R were observed in the CTRL-ECFCs. These results suggest that R reverses long-term ECFC dysfunctions related to IUGR. Full article
(This article belongs to the Special Issue Angiogenic and Pathological Performance of Vascular Endothelial Cells)
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17 pages, 9812 KiB  
Article
Tumor Necrosis Factor Superfamily 14 (LIGHT) Restricts Neovascularization by Decreasing Circulating Endothelial Progenitor Cells and Function
by Chien-Yi Hsu, Chun-Yao Huang, Chun-Ming Shih, Yi-Wen Lin, Po-Hsun Huang, Shing-Jong Lin, Chen-Wei Liu, Cheng-Yen Lin and Feng-Yen Lin
Int. J. Mol. Sci. 2023, 24(8), 6997; https://doi.org/10.3390/ijms24086997 - 10 Apr 2023
Cited by 2 | Viewed by 2211
Abstract
Tumor necrosis factor superfamily 14 (TNFSF14) is also known as the LT-related inducible ligand (LIGHT). It can bind to the herpesvirus invasion mediator and lymphotoxin-β receptor to perform its biological activity. LIGHT has multiple physiological functions, including strengthening the synthesis of nitric oxide, [...] Read more.
Tumor necrosis factor superfamily 14 (TNFSF14) is also known as the LT-related inducible ligand (LIGHT). It can bind to the herpesvirus invasion mediator and lymphotoxin-β receptor to perform its biological activity. LIGHT has multiple physiological functions, including strengthening the synthesis of nitric oxide, reactive oxygen species, and cytokines. LIGHT also stimulates angiogenesis in tumors and induces the synthesis of high endothelial venules; degrades the extracellular matrix in thoracic aortic dissection, and induces the expression of interleukin-8, cyclooxygenase-2, and cell adhesion molecules in endothelial cells. While LIGHT induces tissue inflammation, its effects on angiogenesis after tissue ischemia are unclear. Thus, we analyzed these effects in the current study. In this study, the animal model of hind limb ischemia surgery in C57BL/6 mice was performed. Doppler ultrasound, immunohistochemical staining, and Western blotting were employed to analyze the situation of angiogenesis. In addition, human endothelial progenitor cells (EPCs) were used for in vitro studies to analyze the possible mechanisms. The results in the animal study showed that LIGHT injection inhibited angiogenesis in ischemic limbs. For the in vitro studies, LIGHT inhibited the expression of integrins and E-selectin; decreased migration and tube formation capabilities, mitochondrial respiration, and succinate dehydrogenase activity; and promoted senescence in EPCs. Western blotting revealed that the impairment of EPC function by LIGHT may be due to its effects on the proper functioning of the intracellular Akt signaling pathway, endothelial nitrite oxide synthase (eNOS), and mitochondrial respiration. In conclusion, LIGHT inhibits angiogenesis after tissue ischemia. This may be related to the clamped EPC function. Full article
(This article belongs to the Special Issue Angiogenic and Pathological Performance of Vascular Endothelial Cells)
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