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      Endothelial–Vascular Smooth Muscle Cells Interactions in Atherosclerosis

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          Abstract

          Atherosclerosis is a chronic progressive inflammatory process that can eventually lead to cardiovascular disease (CVD). Despite available treatment, the prevalence of atherosclerotic CVD, which has become the leading cause of death worldwide, persists. Identification of new mechanisms of atherogenesis are highly needed in order to develop an effective therapeutic treatment. The blood vessels contain two primary major cell types: endothelial cells (EC) and vascular smooth muscle cells (VSMC). Each of these performs an essential function in sustaining vascular homeostasis. EC-VSMC communication is essential not only to development, but also to the homeostasis of mature blood vessels. Aberrant EC-VSMC interaction could promote atherogenesis. Identification of the mode of EC-VSMC crosstalk that regulates vascular functionality and sustains homeostasis may offer strategic insights for prevention and treatment of atherosclerotic CVD. Here we will review the molecular mechanisms underlying the interplay between EC and VSMC that could contribute to atherosclerosis. We also highlight open questions for future research directions.

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          Most cited references 94

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          Endothelial extracellular matrix: biosynthesis, remodeling, and functions during vascular morphogenesis and neovessel stabilization.

          The extracellular matrix (ECM) is critical for all aspects of vascular biology. In concert with supporting cells, endothelial cells (ECs) assemble a laminin-rich basement membrane matrix that provides structural and organizational stability. During the onset of angiogenesis, this basement membrane matrix is degraded by proteinases, among which membrane-type matrix metalloproteinases (MT-MMPs) are particularly significant. As angiogenesis proceeds, ECM serves essential functions in supporting key signaling events involved in regulating EC migration, invasion, proliferation, and survival. Moreover, the provisional ECM serves as a pliable scaffold wherein mechanical guidance forces are established among distal ECs, thereby providing organizational cues in the absence of cell-cell contact. Finally, through specific integrin-dependent signal transduction pathways, ECM controls the EC cytoskeleton to orchestrate the complex process of vascular morphogenesis by which proliferating ECs organize into multicellular tubes with functional lumens. Thus, the composition of ECM and therefore the regulation of ECM degradation and remodeling serves pivotally in the control of lumen and tube formation and, finally, neovessel stability and maturation.
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            The control of vascular integrity by endothelial cell junctions: molecular basis and pathological implications.

            Human pathologies such as vascular malformations, hemorrhagic stroke, and edema have been associated with defects in the organization of endothelial cell junctions. Understanding the molecular basis of these diseases requires different integrated approaches which include basic cell biology, clinical studies, and studies in animal models such as mice and zebrafish. In this review we discuss recent findings derived from these approaches and their possible integration in a common picture.
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              MicroRNA Regulation of Atherosclerosis.

              Atherosclerosis and its attendant clinical complications, such as myocardial infarction, stroke, and peripheral artery disease, are the leading cause of morbidity and mortality in Western societies. In response to biochemical and biomechanical stimuli, atherosclerotic lesion formation occurs from the participation of a range of cell types, inflammatory mediators, and shear stress. Over the past decade, microRNAs (miRNAs) have emerged as evolutionarily conserved, noncoding small RNAs that serve as important regulators and fine-tuners of a range of pathophysiological cellular effects and molecular signaling pathways involved in atherosclerosis. Accumulating studies reveal the importance of miRNAs in regulating key signaling and lipid homeostasis pathways that alter the balance of atherosclerotic plaque progression and regression. In this review, we highlight current paradigms of miRNA-mediated effects in atherosclerosis progression and regression. We provide an update on the potential use of miRNAs diagnostically for detecting increasing severity of coronary disease and clinical events. Finally, we provide a perspective on therapeutic opportunities and challenges for miRNA delivery in the field.
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                Author and article information

                Contributors
                Journal
                Front Cardiovasc Med
                Front Cardiovasc Med
                Front. Cardiovasc. Med.
                Frontiers in Cardiovascular Medicine
                Frontiers Media S.A.
                2297-055X
                23 October 2018
                2018
                : 5
                Affiliations
                1Department of Medicine, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center , Oklahoma, OK, United States
                2Office of Research Administration, University of Oklahoma Health Sciences Center , Oklahoma, OK, United States
                Author notes

                Edited by: Hong Chen, Harvard Medical School, United States

                Reviewed by: Shiyou Chen, University of Georgia, United States; Wenbo Zhang, The University of Texas Medical Branch at Galveston, United States

                *Correspondence: Jian Xu jian-xu@ 123456ouhsc.edu

                This article was submitted to Atherosclerosis and Vascular Medicine, a section of the journal Frontiers in Cardiovascular Medicine

                Article
                10.3389/fcvm.2018.00151
                6207093
                Copyright © 2018 Li, Qian, Kyler and Xu.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 119, Pages: 8, Words: 6872
                Funding
                Funded by: National Institutes of Health 10.13039/100000002
                Award ID: R01HL-130845
                Funded by: Presbyterian Health Foundation 10.13039/100001298
                Funded by: Oklahoma Center for the Advancement of Science and Technology 10.13039/100008569
                Award ID: HR17-046
                Categories
                Cardiovascular Medicine
                Review

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