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Special Issue "Cell-cell Interactions in Blood Vessels"

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 (30 September 2017) | Viewed by 15787

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 a pathological setting, such as monocytes attaching as in the first stage of atherogenesis, cancer cells and metastasis of these cells to distant locations from the primary tumor, 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 and chemical mediators, such as chemotactic agents that recruit the cells to a particular area along the blood vessel wall, receptors, and ligands that cause the cells to adhere, as well as other factors that cause cells to migrate across the endothelial barrier, and 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 on novel therapeutic interventions in regulating these processes.

Prof. Dr. Richard L. Hoover
Guest Editor

Manuscript Submission Information

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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

Published Papers (5 papers)

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Research

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Article
Differential Effects of sEH Inhibitors on the Proliferation and Migration of Vascular Smooth Muscle Cells
Int. J. Mol. Sci. 2017, 18(12), 2683; https://doi.org/10.3390/ijms18122683 - 11 Dec 2017
Cited by 10 | Viewed by 2357
Abstract
Epoxyeicosatrienoic acid (EET) is a cardioprotective metabolite of arachidonic acid. It is known that soluble epoxide hydrolase (sEH) is involved in the metabolic degradation of EET. The abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) play important roles in the pathogenesis [...] Read more.
Epoxyeicosatrienoic acid (EET) is a cardioprotective metabolite of arachidonic acid. It is known that soluble epoxide hydrolase (sEH) is involved in the metabolic degradation of EET. The abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) play important roles in the pathogenesis of atherosclerosis and restenosis. Thus, the present study investigated the effects of the sEH inhibitor 12-(((tricyclo(3.3.1.13,7)dec-1-ylamino)carbonyl)amino)-dodecanoic acid (AUDA) on platelet-derived growth factor (PDGF)-induced proliferation and migration in rat VSMCs. AUDA significantly inhibited PDGF-induced rat VSMC proliferation, which coincided with Pin1 suppression and heme oxygenase-1 (HO-1) upregulation. However, exogenous 8,9-EET, 11,12-EET, and 14,15-EET treatments did not alter Pin1 or HO-1 levels and had little effect on the proliferation of rat VSMCs. On the other hand, AUDA enhanced the PDGF-stimulated cell migration of rat VSMCs. Furthermore, AUDA-induced activation of cyclooxygenase-2 (COX-2) and subsequent thromboxane A2 (TXA2) production were required for the enhanced migration. Additionally, EETs increased COX-2 expression but inhibited the migration of rat VSMCs. In conclusion, the present study showed that AUDA exerted differential effects on the proliferation and migration of PDGF-stimulated rat VSMCs and that these results may not depend on EET stabilization. Full article
(This article belongs to the Special Issue Cell-cell Interactions in Blood Vessels)
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Article
Subcellular Interactions during Vascular Morphogenesis in 3D Cocultures between Endothelial Cells and Fibroblasts
Int. J. Mol. Sci. 2017, 18(12), 2590; https://doi.org/10.3390/ijms18122590 - 01 Dec 2017
Cited by 7 | Viewed by 2293
Abstract
Background: Increasing the complexity of in vitro systems to mimic three-dimensional tissues and the cellular interactions within them will increase the reliability of data that were previously collected with in vitro systems. In vivo vascularization is based on complex and clearly defined cell–matrix [...] Read more.
Background: Increasing the complexity of in vitro systems to mimic three-dimensional tissues and the cellular interactions within them will increase the reliability of data that were previously collected with in vitro systems. In vivo vascularization is based on complex and clearly defined cell–matrix and cell–cell interactions, where the extracellular matrix (ECM) seems to play a very important role. The aim of this study was to monitor and visualize the subcellular and molecular interactions between endothelial cells (ECs), fibroblasts, and their surrounding microenvironment during vascular morphogenesis in a three-dimensional coculture model. Methods: Quantitative and qualitative analyses during the generation of a coculture tissue construct consisting of endothelial cells and fibroblasts were done using transmission electron microscopy and immunohistochemistry. Results: Dynamic interactions were found in cocultures between ECs, between fibroblasts (FBs), between ECs and FBs, and between the cells and the ECM. Microvesicles were involved in intercellular information transfer. FBs took an active and physical part in the angiogenesis process. The ECM deposited by the cells triggered endothelial angiogenic activity. Capillary-like tubular structures developed and matured. Moreover, some ECM assembled into a basement membrane (BM) having three different layers equivalent to those seen in vivo. Finally, the three-dimensional in vitro construct mirrored the topography of histological tissue sections. Conclusion: Our results visualize the importance of the physical contact between all cellular and acellular components of the cocultures. Full article
(This article belongs to the Special Issue Cell-cell Interactions in Blood Vessels)
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Article
The Specific Mitogen- and Stress-Activated Protein Kinase MSK1 Inhibitor SB-747651A Modulates Chemokine-Induced Neutrophil Recruitment
Int. J. Mol. Sci. 2017, 18(10), 2163; https://doi.org/10.3390/ijms18102163 - 17 Oct 2017
Cited by 4 | Viewed by 2310
Abstract
Mitogen-activated protein kinase (MAPK) signaling is involved in a variety of cellular functions. MAPK-dependent functions rely on phosphorylation of target proteins such as mitogen- and stress-activated protein kinase 1 (MSK1). MSK1 participates in the early gene expression and in the production of pro- [...] Read more.
Mitogen-activated protein kinase (MAPK) signaling is involved in a variety of cellular functions. MAPK-dependent functions rely on phosphorylation of target proteins such as mitogen- and stress-activated protein kinase 1 (MSK1). MSK1 participates in the early gene expression and in the production of pro- and anti-inflammatory cytokines. However, the role of MSK1 in neutrophil recruitment remains elusive. Here, we show that chemokine macrophage inflammatory protein-2 (CXCL2) enhances neutrophil MSK1 expression. Using intravital microscopy and time-lapsed video analysis of cremasteric microvasculature in mice, we studied the effect of pharmacological suppression of MSK1 by SB-747651A on CXCL2-elicited neutrophil recruitment. SB-747651A treatment enhanced CXCL2-induced neutrophil adhesion while temporally attenuating neutrophil emigration. CXCL2-induced intraluminal crawling was reduced following SB-747651A treatment. Fluorescence-activated cell sorting analysis of integrin expression revealed that SB-747651A treatment attenuated neutrophil integrin αMβ2 (Mac-1) expression following CXCL2 stimulation. Both the transmigration time and detachment time of neutrophils from the venule were increased following SB-747651A treatment. It also decreased the velocity of neutrophil migration in cremasteric tissue in CXCL2 chemotactic gradient. SB-747651A treatment enhanced the extravasation of neutrophils in mouse peritoneal cavity not at 1–2 h but at 3–4 h following CXCL2 stimulation. Collectively, our data suggest that inhibition of MSK1 by SB-747651A treatment affects CXCL2-induced neutrophil recruitment by modulating various steps of the recruitment cascade in vivo. Full article
(This article belongs to the Special Issue Cell-cell Interactions in Blood Vessels)
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Article
Interleukin 17A Promotes Lymphocytes Adhesion and Induces CCL2 and CXCL1 Release from Brain Endothelial Cells
Int. J. Mol. Sci. 2017, 18(5), 1000; https://doi.org/10.3390/ijms18051000 - 08 May 2017
Cited by 40 | Viewed by 3219
Abstract
The nature of the interaction between Th17 cells and the blood–brain barrier (BBB) is critical for the development of autoimmune inflammation in the central nervous system (CNS). Tumor necrosis factor alpha (TNF-α) or interleukin 17 (IL-17) stimulation is known to enhance the adherence [...] Read more.
The nature of the interaction between Th17 cells and the blood–brain barrier (BBB) is critical for the development of autoimmune inflammation in the central nervous system (CNS). Tumor necrosis factor alpha (TNF-α) or interleukin 17 (IL-17) stimulation is known to enhance the adherence of Th17 cells to the brain endothelium. The brain endothelial cells (bEnd.3) express Vascular cell adhesion molecule 1 (VCAM-1), the receptor responsible for inflammatory cell adhesion, which binds very late antigen 4 (VLA-4) on migrating effector lymphocytes at the early stage of brain inflammation. The present study examines the effect of the pro-inflammatory cytokines TNF-α and IL-17 on the adherence of Th17 cells to bEnd.3. The bEnd.3 cells were found to increase production of CCL2 and CXCL1 after stimulation by pro-inflammatory cytokines, while CCL2, CCL5, CCL20 and IL17 induced Th17 cell migration through a bEnd.3 monolayer. This observation may suggest potential therapeutic targets for the prevention of autoimmune neuroinflammation development in the CNS. Full article
(This article belongs to the Special Issue Cell-cell Interactions in Blood Vessels)
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Review

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Review
The Role of Gap Junction-Mediated Endothelial Cell–Cell Interaction in the Crosstalk between Inflammation and Blood Coagulation
Int. J. Mol. Sci. 2017, 18(11), 2254; https://doi.org/10.3390/ijms18112254 - 27 Oct 2017
Cited by 35 | Viewed by 5246
Abstract
Endothelial cells (ECs) play a pivotal role in the crosstalk between blood coagulation and inflammation. Endothelial cellular dysfunction underlies the development of vascular inflammatory diseases. Recent studies have revealed that aberrant gap junctions (GJs) and connexin (Cx) hemichannels participate in the progression of [...] Read more.
Endothelial cells (ECs) play a pivotal role in the crosstalk between blood coagulation and inflammation. Endothelial cellular dysfunction underlies the development of vascular inflammatory diseases. Recent studies have revealed that aberrant gap junctions (GJs) and connexin (Cx) hemichannels participate in the progression of cardiovascular diseases such as cardiac infarction, hypertension and atherosclerosis. ECs can communicate with adjacent ECs, vascular smooth muscle cells, leukocytes and platelets via GJs and Cx channels. ECs dynamically regulate the expression of numerous Cxs, as well as GJ functionality, in the context of inflammation. Alterations to either result in various side effects across a wide range of vascular functions. Here, we review the roles of endothelial GJs and Cx channels in vascular inflammation, blood coagulation and leukocyte adhesion. In addition, we discuss the relevant molecular mechanisms that endothelial GJs and Cx channels regulate, both the endothelial functions and mechanical properties of ECs. A better understanding of these processes promises the possibility of pharmacological treatments for vascular pathogenesis. Full article
(This article belongs to the Special Issue Cell-cell Interactions in Blood Vessels)
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