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Cell and Molecular Interactions in Blood Vessels 2021
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Cell and Molecular Interactions in Blood Vessels 2021

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 (1 September 2021) | Viewed by 6187

Special Issue Editor

Prof. Dr. Richard L. Hoover

E-Mail Website
Guest Editor
Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-2561, USA
Interests: endothelial stem cell; endothelial cells; receptor; glomerular mesangial cells
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Many different types of cells flow through blood vessels without consequence; however, during certain conditions, some of these cells may initiate an interaction with the endothelial lining and, in doing so, change the microenvironment. The result can be a normal response, such as leukocytes initiating the acute inflammatory response in response to an injury, but they can also result in establishing a pathological setting, such as monocytes attachment in the first stage of atherogenesis, cancer cells and their metastasis to distant locations from the primary tumor, the continuous influx of leukocytes and chronic inflammation, and stem cells affecting wound repair. Research has shown there are many factors involved in these processes evoking different mechanisms—physical factors such as blood flow, chemical mediators such as chemotactic agents that recruit cells to a particular area along the blood vessel wall, and receptors and ligands that cause cells to adhere as well as other factors that cause cells to migrate across the endothelial barrier in addition to factors that result in signaling cascades that permit further migration, proliferation, and repair of blood vessels. In this Special Issue, we will try to provide a summary of these particular cells interacting with the endothelial lining of blood vessels and the implication of those interactions, including recent research findings in these areas. Understanding these interactions could have implications for novel therapeutic interventions in regulating these processes.

Prof. Dr. Richard L. Hoover
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.

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Keywords

  • leukocytes
  • blood flow
  • adhesion molecules
  • metastatic cells
  • atherogenesis
  • transmigration
  • chemokines
  • cytokines
  • cell–cell communication
  • signaling molecules and pathways
  • wound repair
  • endothelial stem cells
  • extracellular matrix

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Published Papers (2 papers)

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Research

11 pages, 2993 KiB  
Article
CD93 Signaling via Rho Proteins Drives Cytoskeletal Remodeling in Spreading Endothelial Cells
by Stefano Barbera, Luisa Raucci, Roberta Lugano, Gian Marco Tosi, Anna Dimberg, Annalisa Santucci, Federico Galvagni and Maurizio Orlandini
Int. J. Mol. Sci. 2021, 22(22), 12417; https://doi.org/10.3390/ijms222212417 - 17 Nov 2021
Cited by 16 | Viewed by 3207
Abstract
During angiogenesis, cell adhesion molecules expressed on the endothelial cell surface promote the growth and survival of newly forming vessels. Hence, elucidation of the signaling pathways activated by cell-to-matrix adhesion may assist in the discovery of new targets to be used in antiangiogenic [...] Read more.
During angiogenesis, cell adhesion molecules expressed on the endothelial cell surface promote the growth and survival of newly forming vessels. Hence, elucidation of the signaling pathways activated by cell-to-matrix adhesion may assist in the discovery of new targets to be used in antiangiogenic therapy. In proliferating endothelial cells, the single-pass transmembrane glycoprotein CD93 has recently emerged as an important endothelial cell adhesion molecule regulating vascular maturation. In this study, we unveil a signaling pathway triggered by CD93 that regulates actin cytoskeletal dynamics responsible of endothelial cell adhesion. We show that the Src-dependent phosphorylation of CD93 and the adaptor protein Cbl leads to the recruitment of Crk, which works as a downstream integrator in the CD93-mediated signaling. Moreover, confocal microscopy analysis of FRET-based biosensors shows that CD93 drives the coordinated activation of Rac1 and RhoA at the cell edge of spreading cells, thus promoting the establishment of cell polarity and adhesion required for cell motility. Full article
(This article belongs to the Special Issue Cell and Molecular Interactions in Blood Vessels 2021)
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18 pages, 38385 KiB  
Article
Cyclophilin D Regulates the Nuclear Translocation of AIF, Cardiac Endothelial Cell Necroptosis and Murine Cardiac Transplant Injury
by Adnan Qamar, Jianqi Zhao, Laura Xu, Patrick McLeod, Xuyan Huang, Jifu Jiang, Weihua Liu, Aaron Haig and Zhu-Xu Zhang
Int. J. Mol. Sci. 2021, 22(20), 11038; https://doi.org/10.3390/ijms222011038 - 13 Oct 2021
Cited by 7 | Viewed by 2420
Abstract
Ischemia-reperfusion injury (IRI) is an inevitable consequence of organ transplant procedure and associated with acute and chronic organ rejection in transplantation. IRI leads to various forms of programmed cell death, which worsens tissue damage and accelerates transplant rejection. We recently demonstrated that necroptosis [...] Read more.
Ischemia-reperfusion injury (IRI) is an inevitable consequence of organ transplant procedure and associated with acute and chronic organ rejection in transplantation. IRI leads to various forms of programmed cell death, which worsens tissue damage and accelerates transplant rejection. We recently demonstrated that necroptosis participates in murine cardiac microvascular endothelial cell (MVEC) death and murine cardiac transplant rejection. However, MVEC death under a more complex IRI model has not been studied. In this study, we found that simulating IRI conditions in vitro by hypoxia, reoxygenation and treatment with inflammatory cytokines induced necroptosis in MVECs. Interestingly, the apoptosis-inducing factor (AIF) translocated to the nucleus during MVEC necroptosis, which is regulated by the mitochondrial permeability molecule cyclophilin D (CypD). Furthermore, CypD deficiency in donor cardiac grafts inhibited AIF translocation and mitigated graft IRI and rejection (n = 7; p = 0.002). Our studies indicate that CypD and AIF play significant roles in MVEC necroptosis and cardiac transplant rejection following IRI. Targeting CypD and its downstream AIF may be a plausible approach to inhibit IRI-caused cardiac damage and improve transplant survival. Full article
(This article belongs to the Special Issue Cell and Molecular Interactions in Blood Vessels 2021)
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