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Cell and Molecular Interactions in Blood Vessels

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

Deadline for manuscript submissions: closed (25 September 2019) | Viewed by 21130

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Special Issue Editor

Prof. Dr. Richard L. Hoover

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Guest Editor

Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-2561, USA
Interests: cell-cell interactions; vascular biology; endothelial cell biology; inflammation

Special Issue Information

Dear Colleagues,

Many different types of cells flow through blood vessels without consequence; however, under certain conditions, the cells change from a non-interactive type to one that causes the cells to adhere to themselves or to other cells in this microenvironment. As a result of this, an inflammatory response, athrogenesis, clotting, and metastasis of cancer cells is initiated. There are many mediators of this cellular change causing the cells to adhere, clump, or migrate along and/or into the blood vessel wall. The mediators are quite varied, and the responses to them are just as varied. Some cause the cells to become adhesive, others cause the cells to be non-adhesive; some cause the cells to change morphology in order to make the cell wall more permeable, which in turn can affect migration through the wall. The response to these mediators and the adhesion to other cells affect the cells by initiating various signaling pathways, and, depending on the pathway, the function of the cells is affected in a different manner. In this Special Issue, we will try to provide a summary of how all these different cells interact, what mediates these effects, and how these effects are initiated and propagated. Understanding these interactions could have implications for novel therapeutic interventions to regulate these processes when they go awry.

Prof. Dr. Richard L. Hoover
Guest Editor

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Keywords

endothelial cells
leukocytes
platelets
small molecule mediators
lipid mediators
growth factors
signaling molecules
adhesion
migration
metastasis

Published Papers (5 papers)

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Research

17 pages, 9221 KiB

Open AccessArticle

Four Cysteine Residues Contribute to Homodimerization of Chicken Interleukin-2

by Chen Deng, Hailiang Tan, Hongda Zhou, Mengyun Wang, Yan Lü, Jiacui Xu, Huanmin Zhang, Limei Han and Yongxing Ai

Int. J. Mol. Sci. 2019, 20(22), 5744; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20225744 - 15 Nov 2019

Cited by 1 | Viewed by 2545

Abstract

Interleukin-2 (IL-2) is a pleiotropic cytokine regulating the immune and nervous systems. Mammalian and bird IL-2s have different protein sequences, but perform similar functions. In the current study, two bands were detected by immunoblotting using an antibody against freshly purified chicken IL-2 (chIL-2). The molecular weight of the larger band was approximately twice as much of the chIL-2 monomer, although a chIL-2 complex or homodimer has never been reported. To explain this intriguing result, several dissociation reagents were used to examine the intermolecular forces between components of the proposed chIL-2 complex. It was found that intermolecular disulphide bond promotes homodimerization of chIL-2. Subsequently, mutation of Cys residues of chIL-2 revealed that mutation of all four Cys residues disrupted homodimerization, but a single, dual, or triple Cys mutation failed to disrupt homodimerization, suggesting that all four Cys residues on chIL-2 contribute to this dimerization. Functional analysis showed that both monomeric and dimeric chIL-2 consisting of either wild type or mutant chIL-2 were able to stimulate the expansion of CD4⁺ T cell in vivo or in vitro, and effectively bind to chIL-2 receptor. Overall, this study revealed that the recombinant chIL-2 purified from either Escherichia coli (E. coli) or Spodoptera frugiperda (Sf9) cells could homodimerize in vitro, with all four Cys residues on each chIL-2 protein contributing to this homodimerization, and dimerization and Cys mutation not impacting chIL-2 induced stimulation of chicken CD4⁺ T cells. Full article

(This article belongs to the Special Issue Cell and Molecular Interactions in Blood Vessels)

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19 pages, 3346 KiB

Open AccessArticle

MMP-12, Secreted by Pro-Inflammatory Macrophages, Targets Endoglin in Human Macrophages and Endothelial Cells

by Mikel Aristorena, Eunate Gallardo-Vara, Matej Vicen, Mateo de Las Casas-Engel, Luisa Ojeda-Fernandez, Concepción Nieto, Francisco J. Blanco, Ana C. Valbuena-Diez, Luisa M. Botella, Petr Nachtigal, Angel L. Corbi, María Colmenares and Carmelo Bernabeu

Int. J. Mol. Sci. 2019, 20(12), 3107; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20123107 - 25 Jun 2019

Cited by 51 | Viewed by 6713

Abstract

Upon inflammation, monocyte-derived macrophages (MΦ) infiltrate blood vessels to regulate several processes involved in vascular pathophysiology. However, little is known about the mediators involved. Macrophage polarization is crucial for a fast and efficient initial response (GM-MΦ) and a good resolution (M-MΦ) of the inflammatory process. The functional activity of polarized MΦ is exerted mainly through their secretome, which can target other cell types, including endothelial cells. Endoglin (CD105) is a cell surface receptor expressed by endothelial cells and MΦ that is markedly upregulated in inflammation and critically involved in angiogenesis. In addition, a soluble form of endoglin with anti-angiogenic activity has been described in inflammation-associated pathologies. The aim of this work was to identify components of the MΦ secretome involved in the shedding of soluble endoglin. We find that the GM-MΦ secretome contains metalloprotease 12 (MMP-12), a GM-MΦ specific marker that may account for the anti-angiogenic activity of the GM-MΦ secretome. Cell surface endoglin is present in both GM-MΦ and M-MΦ, but soluble endoglin is only detected in GM-MΦ culture supernatants. Moreover, MMP-12 is responsible for the shedding of soluble endoglin in vitro and in vivo by targeting membrane-bound endoglin in both MΦ and endothelial cells. These data demonstrate a direct correlation between GM-MΦ polarization, MMP-12, and soluble endoglin expression and function. By targeting endothelial cells, MMP-12 may represent a novel mediator involved in vascular homeostasis. Full article

(This article belongs to the Special Issue Cell and Molecular Interactions in Blood Vessels)

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18 pages, 1889 KiB

Open AccessArticle

Bioinformatic Analysis of Gene Variants from Gastroschisis Recurrence Identifies Multiple Novel Pathogenetic Pathways: Implication for the Closure of the Ventral Body Wall

by Víctor M. Salinas-Torres, Hugo L. Gallardo-Blanco, Rafael A. Salinas-Torres, Ricardo M. Cerda-Flores, José J. Lugo-Trampe, Daniel Z. Villarreal-Martínez and Laura E. Martínez de Villarreal

Int. J. Mol. Sci. 2019, 20(9), 2295; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20092295 - 09 May 2019

Cited by 10 | Viewed by 3944

Abstract

We investigated whether likely pathogenic variants co-segregating with gastroschisis through a family-based approach using bioinformatic analyses were implicated in body wall closure. Gene Ontology (GO)/Panther functional enrichment and protein-protein interaction analysis by String identified several biological networks of highly connected genes in UGT1A3, UGT1A4, UGT1A5, UGT1A6, UGT1A7, UGT1A8, UGT1A9, UGT1A10, AOX1, NOTCH1, HIST1H2BB, RPS3, THBS1, ADCY9, and FGFR4. SVS–PhoRank identified a dominant model in OR10G4 (also as heterozygous de novo), ITIH3, PLEKHG4B, SLC9A3, ITGA2, AOX1, and ALPP, including a recessive model in UGT1A7, UGT1A6, PER2, PTPRD, and UGT1A3. A heterozygous compound model was observed in CDYL, KDM5A, RASGRP1, MYBPC2, PDE4DIP, F5, OBSCN, and UGT1A. These genes were implicated in pathogenetic pathways involving the following GO related categories: xenobiotic, regulation of metabolic process, regulation of cell adhesion, regulation of gene expression, inflammatory response, regulation of vascular development, keratinization, left-right symmetry, epigenetic, ubiquitination, and regulation of protein synthesis. Multiple background modifiers interacting with disease-relevant pathways may regulate gastroschisis susceptibility. Based in our findings and considering the plausibility of the biological pattern of mechanisms and gene network modeling, we suggest that the gastroschisis developmental process may be the consequence of several well-orchestrated biological and molecular mechanisms which could be interacting with gastroschisis predispositions within the first ten weeks of development. Full article

(This article belongs to the Special Issue Cell and Molecular Interactions in Blood Vessels)

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12 pages, 1808 KiB

Open AccessArticle

Calcium Release from Endoplasmic Reticulum Involves Calmodulin-Mediated NADPH Oxidase-Derived Reactive Oxygen Species Production in Endothelial Cells

by Ryugo Sakurada, Keiichi Odagiri, Akio Hakamata, Chiaki Kamiya, Jiazhang Wei and Hiroshi Watanabe

Int. J. Mol. Sci. 2019, 20(7), 1644; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20071644 - 02 Apr 2019

Cited by 14 | Viewed by 3948

Abstract

Background: Previous studies demonstrated that calcium/calmodulin (Ca²⁺/CaM) activates nicotinamide adenine dinucleotide phosphate oxidases (NOX). In endothelial cells, the elevation of intracellular Ca²⁺ level consists of two components: Ca²⁺ mobilization from the endoplasmic reticulum (ER) and the subsequent store-operated Ca²⁺ entry. However, little is known about which component of Ca²⁺ increase is required to activate NOX in endothelial cells. Here, we investigated the mechanism that regulates NOX-derived reactive oxygen species (ROS) production via a Ca²⁺/CaM-dependent pathway. Methods: We measured ROS production using a fluorescent indicator in endothelial cells and performed phosphorylation assays. Results: Bradykinin (BK) increased NOX-derived cytosolic ROS. When cells were exposed to BK with either a nominal Ca²⁺-free or 1 mM of extracellular Ca²⁺ concentration modified Tyrode’s solution, no difference in BK-induced ROS production was observed; however, chelating of cytosolic Ca²⁺ by BAPTA/AM or the depletion of ER Ca²⁺ contents by thapsigargin eliminated BK-induced ROS production. BK-induced ROS production was inhibited by a CaM inhibitor; however, a Ca²⁺/CaM-dependent protein kinase II (CaMKII) inhibitor did not affect BK-induced ROS production. Furthermore, BK stimulation did not increase phosphorylation of NOX2, NOX4, and NOX5. Conclusions: BK-induced NOX-derived ROS production was mediated via a Ca²⁺/CaM-dependent pathway; however, it was independent from NOX phosphorylation. This was strictly regulated by ER Ca²⁺ contents. Full article

(This article belongs to the Special Issue Cell and Molecular Interactions in Blood Vessels)

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12 pages, 2447 KiB

Open AccessArticle

Vascular Effects of Photodynamic Therapy with Curcumin in a Chorioallantoic Membrane Model

by Hilde Harb Buzzá, Lucas Cruz Fialho de Freitas, Lilian Tan Moriyama, Ramon Gabriel Teixeira Rosa, Vanderlei Salvador Bagnato and Cristina Kurachi

Int. J. Mol. Sci. 2019, 20(5), 1084; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms20051084 - 02 Mar 2019

Cited by 22 | Viewed by 3545

Abstract

Photodynamic Therapy (PDT) is a treatment that requires light, a photosensitizing agent, and molecular oxygen. The photosensitizer is activated by light and it interacts with the oxygen that is present in the cellular microenvironment. The molecular oxygen is transformed into singlet oxygen, which is highly reactive and responsible for the cell death. Therefore, PS is an important element for the therapy happens, including its concentration. Curcumin is a natural photosensitizer and it has demonstrated its anti-inflammatory and anti-oxidant effects that inhibit several signal transduction pathways. PDT vascular effects of curcumin at concentrations varying from 0.1 to 10 mM/cm² and topical administration were investigated in a chick Chorioallantoic Membrane (CAM) model. The irradiation was performed at 450 nm, irradiance of 50 mW/cm² during 10 min, delivering a total fluence of 30 J/cm². The vascular effect was followed after the application of curcumin, with images being obtained each 30 min in the first 3 h, 12 h, and 24 h. Those images were qualitatively and quantitatively analyzed with a MatLAB^®. Curcumin was expected to exhibit a vascular effect due to its angio-inhibitory effect. Using curcumin as photosensitizer, PDT induced a higher and faster vascular effect when compared to the use of this compound alone. Full article

(This article belongs to the Special Issue Cell and Molecular Interactions in Blood Vessels)

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