Special Issue "Cell Adhesion Molecules"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Motility and Adhesion".

Deadline for manuscript submissions: 30 November 2018

Special Issue Editor

Guest Editor
Dr. Ann Hopkins

Royal College of Surgeons in Ireland, Department of Surgery, Dublin, Ireland
Website | E-Mail
Phone: +35318093858
Interests: tight junctions; adhesion; tumorigenesis; Junctional Adhesion Molecule-A (JAM-A); breast cancer

Special Issue Information

Dear Colleagues,

Cell adhesion molecules are fundamental regulators of the structure and function of most tissues and organs. Their numerous physiological roles have expanded over recent decades to include the regulation of barrier function, polarity, cell-cell and cell-matrix communication, neural transmission, stem cell renewal, cell division and immune function to name but a few. Pathophysiologically speaking, dysregulation of adhesion molecule signaling has been implicated in conditions from cancer to inflammation to cognitive impairment. This Special Issue of Cells will advance our understanding of the upstream regulators and downstream targets of cell adhesion molecules, and the cellular mechanisms allowing them act as active drivers of various physiological and pathophysiological processes. Original contributions are welcome from authors actively engaged in the fields of cell–cell adhesion, cell–matrix adhesion and leukocyte adhesion, as well as from authors interested in emerging adhesion-independent signaling events associated with cell adhesion molecules. All models of study and all disease states will be considered, including systems biology approaches that provide new insight into the fundamental regulation of adhesion signaling.

We look forward to your contributions.

Dr. Ann Hopkins
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 papers will be 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. Cells is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). 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

  • adhesion
  • cell-cell junctions
  • cell-matrix junctions
  • tight junctions
  • adherens junctions
  • intercellular adhesion
  • integrins
  • cell adhesion molecules

Published Papers (6 papers)

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Research

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Open AccessFeature PaperArticle The Desmosomal Cadherin Desmoglein-2 Experiences Mechanical Tension as Demonstrated by a FRET-Based Tension Biosensor Expressed in Living Cells
Received: 10 March 2018 / Revised: 21 June 2018 / Accepted: 22 June 2018 / Published: 26 June 2018
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Abstract
Cell-cell junctions are critical structures in a number of tissues for mechanically coupling cells together, cell-to-cell signaling, and establishing a barrier. In many tissues, desmosomes are an important component of cell-cell junctions. Loss or impairment of desmosomes presents with clinical phenotypes in the
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Cell-cell junctions are critical structures in a number of tissues for mechanically coupling cells together, cell-to-cell signaling, and establishing a barrier. In many tissues, desmosomes are an important component of cell-cell junctions. Loss or impairment of desmosomes presents with clinical phenotypes in the heart and skin as cardiac arrhythmias and skin blistering, respectively. Because heart and skin are tissues that are subject to large mechanical stresses, we hypothesized that desmosomes, similar to adherens junctions, would also experience significant tensile loading. To directly measure mechanical forces across desmosomes, we developed and validated a desmoglein-2 (DSG-2) force sensor, using the existing TSmod Förster resonance energy transfer (FRET) force biosensor. When expressed in human cardiomyocytes, the force sensor reported high tensile loading of DSG-2 during contraction. Additionally, when expressed in Madin-Darby canine kidney (MDCK) epithelial or epidermal (A431) monolayers, the sensor also reported tensile loading. Finally, we observed higher DSG-2 forces in 3D MDCK acini when compared to 2D monolayers. Taken together, our results show that desmosomes experience low levels of mechanical tension in resting cells, with significantly higher forces during active loading. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules)
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Open AccessArticle Cell Adhesion Molecules Are Mediated by Photobiomodulation at 660 nm in Diabetic Wounded Fibroblast Cells
Received: 9 March 2018 / Revised: 9 April 2018 / Accepted: 12 April 2018 / Published: 16 April 2018
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Abstract
Diabetes affects extracellular matrix (ECM) metabolism, contributing to delayed wound healing and lower limb amputation. Application of light (photobiomodulation, PBM) has been shown to improve wound healing. This study aimed to evaluate the influence of PBM on cell adhesion molecules (CAMs) in diabetic
[...] Read more.
Diabetes affects extracellular matrix (ECM) metabolism, contributing to delayed wound healing and lower limb amputation. Application of light (photobiomodulation, PBM) has been shown to improve wound healing. This study aimed to evaluate the influence of PBM on cell adhesion molecules (CAMs) in diabetic wound healing. Isolated human skin fibroblasts were grouped into a diabetic wounded model. A diode laser at 660 nm with a fluence of 5 J/cm2 was used for irradiation and cells were analysed 48 h post-irradiation. Controls consisted of sham-irradiated (0 J/cm2) cells. Real-time reverse transcription (RT) quantitative polymerase chain reaction (qPCR) was used to determine the expression of CAM-related genes. Ten genes were up-regulated in diabetic wounded cells, while 25 genes were down-regulated. Genes were related to transmembrane molecules, cell–cell adhesion, and cell–matrix adhesion, and also included genes related to other CAM molecules. PBM at 660 nm modulated gene expression of various CAMs contributing to the increased healing seen in clinical practice. There is a need for new therapies to improve diabetic wound healing. The application of PBM alongside other clinical therapies may be very beneficial in treatment. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules)
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Open AccessArticle Flotillins Regulate Focal Adhesions by Interacting with α-Actinin and by Influencing the Activation of Focal Adhesion Kinase
Received: 26 February 2018 / Revised: 4 April 2018 / Accepted: 6 April 2018 / Published: 7 April 2018
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Abstract
Cell–matrix adhesion and cell migration are physiologically important processes that also play a major role in cancer spreading. In cultured cells, matrix adhesion depends on integrin-containing contacts such as focal adhesions. Flotillin-1 and flotillin-2 are frequently overexpressed in cancers and are associated with
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Cell–matrix adhesion and cell migration are physiologically important processes that also play a major role in cancer spreading. In cultured cells, matrix adhesion depends on integrin-containing contacts such as focal adhesions. Flotillin-1 and flotillin-2 are frequently overexpressed in cancers and are associated with poor survival. Our previous studies have revealed a role for flotillin-2 in cell–matrix adhesion and in the regulation of the actin cytoskeleton. We here show that flotillins are important for cell migration in a wound healing assay and influence the morphology and dynamics of focal adhesions. Furthermore, anchorage-independent growth in soft agar is enhanced by flotillins. In the absence of flotillins, especially flotillin-2, phosphorylation of focal adhesion kinase and extracellularly regulated kinase is diminished. Flotillins interact with α-actinin, a major regulator of focal adhesion dynamics. These findings are important for understanding the molecular mechanisms of how flotillin overexpression in cancers may affect cell migration and, especially, enhance metastasis formation. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules)
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Review

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Open AccessFeature PaperReview Adhesion in Physiological, Benign and Malignant Proliferative States of the Endometrium: Microenvironment and the Clinical Big Picture
Received: 12 March 2018 / Revised: 9 May 2018 / Accepted: 11 May 2018 / Published: 16 May 2018
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Abstract
Although the developments in cellular and molecular biology over the last few decades have significantly advanced our understanding of the processes and players that regulate invasive disease, many areas of uncertainty remain. This review will discuss the contribution of dysregulated cell–cell and cell–matrix
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Although the developments in cellular and molecular biology over the last few decades have significantly advanced our understanding of the processes and players that regulate invasive disease, many areas of uncertainty remain. This review will discuss the contribution of dysregulated cell–cell and cell–matrix adhesion to the invasion in both benign and malignant contexts. Using the endometrium as an illustrative tissue that undergoes clinically significant invasion in both contexts, the adhesion considerations in the cells (“seed”) and their microenvironment (“soil”) will be discussed. We hope to orientate this discussion towards translational relevance for the diagnosis and treatment of endometrial conditions, which are currently associated with significant morbidity and mortality. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules)
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Open AccessReview Junctional Adhesion Molecules (JAMs): The JAM-Integrin Connection
Received: 27 February 2018 / Revised: 21 March 2018 / Accepted: 24 March 2018 / Published: 26 March 2018
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Abstract
Junctional adhesion molecules (JAMs) are cell surface adhesion receptors of the immunoglobulin superfamily. JAMs are involved in a variety of biological processes both in the adult organism but also during development. These include processes such as inflammation, angiogenesis, hemostasis, or epithelial barrier formation,
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Junctional adhesion molecules (JAMs) are cell surface adhesion receptors of the immunoglobulin superfamily. JAMs are involved in a variety of biological processes both in the adult organism but also during development. These include processes such as inflammation, angiogenesis, hemostasis, or epithelial barrier formation, but also developmental processes such as hematopoiesis, germ cell development, and development of the nervous system. Several of these functions of JAMs depend on a physical and functional interaction with integrins. The JAM – integrin interactions in trans regulate cell-cell adhesion, their interactions in cis regulate signaling processes originating at the cell surface. The JAM – integrin interaction can regulate the function of the JAM as well as the function of the integrin. Beyond the physical interaction with integrins, JAMs can regulate integrin function through intracellular signaling indicating an additional level of JAM – integrin cross-talk. In this review, we describe the various levels of the functional interplay between JAMs and integrins and the role of this interplay during different physiological processes. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules)
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Open AccessReview Integrin Activation: Implications for Axon Regeneration
Received: 4 January 2018 / Revised: 1 March 2018 / Accepted: 9 March 2018 / Published: 10 March 2018
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Abstract
Integrin activation is essential for creating functional transmembrane receptors capable of inducing downstream cellular effects such as cell migration, cell spreading, neurite outgrowth and axon regeneration. Integrins are bidirectional signalling molecules that mediate their effects by ‘inside–out’ and ‘outside–in’ signalling. This review will
[...] Read more.
Integrin activation is essential for creating functional transmembrane receptors capable of inducing downstream cellular effects such as cell migration, cell spreading, neurite outgrowth and axon regeneration. Integrins are bidirectional signalling molecules that mediate their effects by ‘inside–out’ and ‘outside–in’ signalling. This review will provide a detailed overview of integrin activation focusing on intracellular activation in neurons and discussing direct implications in the regulation of neurite outgrowth and axon regeneration. Full article
(This article belongs to the Special Issue Cell Adhesion Molecules)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Authors: Houreld N.N., Ayuk S.M. and Abrahamse H.
Affiliation: Laser Research Centre, Faculty of Health Sciences, University of Johannesburg, P.O. Box 17011, Doornfontein, Johannesburg, 2028, South Africa Tel: +27 11 559-6833 Fax +27 11 559-6884
Tentative title: Cell Adhesion Molecules are Mediated by Photobiomodulation at 660 nm in Diabetic Wounded Fibroblast Cells
Abstract: Diabetes is a metabolic disorder identified by hyperglycaemia. It may affect gene expression and extracellular matrix (ECM) metabolism, contributing to delayed wound healing and leading to chronic ulcers and amputations. Diabetic foot ulcers require extensive treatment and impact heavily on patient’s quality of life. Application of lasers and light (photobiomodulation, PBM) has been shown to improve diabetic wound healing; however, the underlying mechanisms are poorly understood. This study aimed to evaluate the influence of PBM at 660 nm on various cell adhesion molecules (CAMs) in diabetic wound healing. Human skin fibroblasts (WS1) were grouped into three models; normal (unstressed), wounded (stressed) and diabetic wounded (stressed). A continuous wave diode laser at 660 nm with a fluence of 5 J/cm2 was used for irradiation and cells were analysed 48 h post-irradiation. Controls consisted of sham-irradiated (0 J/cm2) cells. Real-time reverse transcription (RT) quantitative polymerase chain reaction (qPCR) was used to determine the expression of a variety of CAM related genes. Thirteen genes were up-regulated in normal cells, 15 in normal wounded cells and 7 in diabetic wounded cells, meanwhile four genes were down-regulated in normal cells, three genes in normal wounded cells, and 11 in diabetic wounded cells. Genes were related to transmembrane molecules, cell-cell adhesion, and cell-matrix adhesion. PBM at 660 nm modulated gene expression of various CAMs contributing to the increased healing seen in clinical practice. There is a need for new therapies to improve diabetic wound healing. The application of PBM alongside other clinical therapies may be very beneficial in treatment.

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