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The Cell Communication in Vascular Biology
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The Cell Communication in Vascular Biology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 2847

Special Issue Editor

Dr. Kapka Miteva

E-Mail Website
Guest Editor
Division of Cardiology, Foundation for Medical Research, Department of Medicine Specialized Medicine, Faculty of Medicine, University of Geneva, Av. de la Roseraie 64, CH-1211 Geneva, Switzerland
Interests: vascular biology; atherosclerosis; vascular calcification
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The aim of the Special Issue, “Cell Communication in Vascular Biology”, is to provide deeper insight into the complex mechanism of signaling between the main cell types in the vasculature in health and pathology. The Special Issue will outline recent advances in our understanding of the multicellular communication between vascular smooth muscle cells, endothelial cells, platelets, and leukocytes.

Different aspects of cell communication will be of interest, including direct cell–cell contact by adhesion molecules or gap junctions; classic receptor-mediated paracrine signaling and intercellular genetic modification by non-coding RNAs as well as microvesicles transfer. The Special Issue will place particular emphasis on exosomes as novel intercellular communication messengers containing biologically active proteins, lipids, and RNA species. The role of exosomes in paracrine or autocrine cell communication in vascular repair, thrombosis, atherosclerosis, and vascular calcification will be of major interest for the Special Issue on “Cell Communication in Vascular Biology” in IJMS.

Dr. Kapka Miteva
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 smooth muscle (VSM)
  • platelets
  • leukocytes
  • endothelial cells
  • macrophages
  • adhesion molecules
  • gap junctions
  • paracrine receptor-mediated signaling
  • non-coding RNAs

Published Papers (1 paper)

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Research

17 pages, 25859 KiB  
Article
Myeloperoxidase-Oxidized LDL Activates Human Aortic Endothelial Cells through the LOX-1 Scavenger Receptor
by Layal El-Hajjar, Judy Hindieh, Rana Andraos, Marwan El-Sabban and Jalil Daher
Int. J. Mol. Sci. 2022, 23(5), 2837; https://doi.org/10.3390/ijms23052837 - 4 Mar 2022
Cited by 6 | Viewed by 2279
Abstract
Cardiovascular disease as a result of atherosclerosis is a leading cause of death worldwide. Atherosclerosis is primarily caused by the dysfunction of vascular endothelial cells and the subendothelial accumulation of oxidized forms of low-density lipoprotein (LDL). Early observations have linked oxidized LDL effects [...] Read more.
Cardiovascular disease as a result of atherosclerosis is a leading cause of death worldwide. Atherosclerosis is primarily caused by the dysfunction of vascular endothelial cells and the subendothelial accumulation of oxidized forms of low-density lipoprotein (LDL). Early observations have linked oxidized LDL effects in atherogenesis to the lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) scavenger receptor. It was shown that LOX-1 is upregulated by many inflammatory mediators and proatherogenic stimuli including cytokines, reactive oxygen species (ROS), hemodynamic blood flow, high blood sugar levels and, most importantly, modified forms of LDL. Oxidized LDL signaling pathways in atherosclerosis were first explored using LDL that is oxidized by copper (Cuox-LDL). In our study, we used a more physiologically relevant model of LDL oxidation and showed, for the first time, that myeloperoxidase oxidized LDL (Mox-LDL) may affect human aortic endothelial cell (HAEC) function through the LOX-1 scavenger receptor. We report that Mox-LDL increases the expression of its own LOX-1 receptor in HAECs, enhancing inflammation and simultaneously decreasing tubulogenesis in the cells. We hypothesize that Mox-LDL drives endothelial dysfunction (ED) through LOX-1 which provides an initial hint to the pathways that are initiated by Mox-LDL during ED and the progression of atherosclerosis. Full article
(This article belongs to the Special Issue The Cell Communication in Vascular Biology)
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