Cell Communication and Adhesion最新文献

Ruta graveolens silver nanoparticles (AgNPs) showed the color change within 30 min and characterized using UV-visible spectra, Fourier Transform Infrared (FTIR), X-ray Diffraction (XRD) and Transmission Electron Microscopy (TEM). UV-visible spectrum of R. graveolens AgNPs showed the sharp peak at the wavelength of 440-560 nm. XRD patterns confirmed that crystalline nature of R. graveolens AgNPs and FTIR results revealed that phytochemical reaction of these R. graveolens is responsible for the synthesis of AgNPs. TEM results showed the size of the R. graveolens AgNPs around 30-50 nm with spherical and triangular nature. Further, the antibacterial and antibiofilm activity of R. graveolens AgNPs showed the effective inhibitory activity against clinically important Staphylococcus aureus, Pseudomonas aeruginosa and Candida albicans. Our findings suggest that R. graveolens AgNPs can be exploited toward the development of potential antibacterial agents for various biomedical and environmental applications.

Cell-to-cell information exchange mediated by membrane protrusions in tunneling nanotubes (TNTs) has been widely described in distinct cell lines. Here, we describe a new form of direct intercellular communication in a murine macrophage-like cell line that is mediated by pseudopodial fusions that form over scraped plastic tissue culture surfaces along scratch lines. These structures are capable of forming intercellular, tunnel-like channels (inter-pseudopodial axis connections) that can be differentiated from TNTs based on length, thickness, tandem arrangement along an axis, pseudopodial origin and permanency. These channels were able to exchange membrane lipids and contain particles 0.5 μm or lesser in diameter between cells and might represent an additional biological function of pseudopodia.

The occurrence of invadopodia has been, since its characterization, a hallmark of cancerous cell invasion and metastasis. These structures are now the subject of a controversy concerning their cellular function, molecular regulation, and assembly. The terms invadopodia and podosomes have been used interchangeably since their discovery back in 1980. Since then, these phenotypes are now more established and accepted by the scientific community as vital structures for 3D cancer cell motility. Many characteristics relating to invadopodia and podosomes have been elucidated, which might prove these structures as good targets for metastasis treatment. In this review, we briefly review the actin reorganization process needed in most types of cancer cell motility. We also review the important characteristics of invadopodia, including molecular components, assembly, markers, and the signaling pathways, providing a comprehensive model for invadopodia regulation.

Cardiac conduction is the propagation of electrical excitation through the heart and is responsible for triggering individual myocytes to contract in synchrony. Canonically, this process has been thought to occur electrotonically, by means of direct flow of ions from cell to cell. The intercalated disk (ID), the site of contact between adjacent myocytes, has been viewed as a structure composed of mechanical junctions that stabilize the apposition of cell membranes and gap junctions which constitute low resistance pathways between cells. However, emerging evidence suggests a more active role for structures within the ID in mediating intercellular electrical communication by means of non-canonical ephaptic mechanisms. This review will discuss the role of the ID in the context of the canonical, electrotonic view of conduction and highlight new, emerging possibilities of its playing a more active role in ephaptic coupling between cardiac myocytes.

Cell Communication and Adhesion has been fortunate to enlist two pioneers of epidermal and cardiac cell junctions, Kathleen Green and Mario Delmar, as Guest Editors of a two part series on junctional targets of skin and heart disease. Part 2 of this series begins with an overview from Dipal Patel and Kathy Green comparing epidermal desmosomes to cardiac area composita junctions, and surveying the pathogenic mechanisms resulting from mutations in their components in heart disease. This is followed by a review from David Kelsell on the role of desmosomal mutation in inherited syndromes involving skin fragility. Agnieszka Kobeliak discusses how structural deficits in the epidermal barrier intersect with the NFkB signaling pathway to induce inflammatory diseases such as psoriasis and atopic dermatitis. Farah Sheikh reviews the specialized junctional components in cardiomyocytes of the cardiac conduction system and Robert Gourdie discusses how molecular complexes between sodium channels and gap junction proteins within the perijunctional microdomains within the intercalated disc facilitate conduction. Glenn Radice evaluates the role of N-cadherin in heart. Andre Kleber and Chris Chen explore new approaches to study junctional mechanotransduction in vitro with a focus on the effects of connexin ablation and the role of cadherins, respectively. To complement this series of reviews, we have interviewed Werner Franke, whose systematic documentation the tissue-specific complexity of desmosome composition and pioneering discovery of the cardiac area composita junction greatly facilitated elucidation of the role of desmosomal components in the pathophysiology of human heart disease.

The importance of desmosomes in tissue homeostasis is highlighted by natural and engineered mutations in desmosomal genes, which compromise the skin or heart and in some instances both. Desmosomal gene mutations account for 45-50% of cases of arrhythmogenic right ventricular cardiomyopathy, and are mutated in an array of other disorders such as striate palmoplantar keratoderma, hypotrichosis with or without skin vesicles and lethal acantholytic epidermolysis bullosa. Recently, we reported loss-of-function mutations in the human ADAM17 gene, encoding for the 'sheddase' ADAM17, a transmembrane protein which cleaves extracellular domains of substrate proteins including TNF-α, growth factors and desmoglein (DSG) 2. Patients present with cardiomyopathy and an inflammatory skin and bowel syndrome with defective DSG processing. In contrast, the dominantly inherited tylosis with oesophageal cancer appears to result from gain-of-function in ADAM17 due to increased processing via iRHOM2. This review discusses the heterogeneity of mutations in desmosomes and their regulatory proteins.

Anchoring cell junctions are integral in maintaining electro-mechanical coupling of ventricular working cardiomyocytes; however, their role in cardiomyocytes of the cardiac conduction system (CCS) remains less clear. Recent studies in genetic mouse models and humans highlight the appearance of these cell junctions alongside gap junctions in the CCS and also show that defects in these structures and their components are associated with conduction impairments in the CCS. Here we outline current evidence supporting an integral relationship between anchoring and gap junctions in the CCS. Specifically we focus on (1) molecular and ultrastructural evidence for cell-cell junctions in specialized cardiomyocytes of the CCS, (2) genetic mouse models specifically targeting cell-cell junction components in the heart which exhibit CCS conduction defects and (3) human clinical studies from patients with cell-cell junction-based diseases that exhibit CCS electrophysiological defects.

The skin forms a life-sustaining barrier between the organism and physical environment. The physical barrier of skin is mainly localized in the stratum corneum (SC); however, nucleated epidermis also contributes to the barrier through tight, gap, and adherens junctions (AJs), as well as through desmosomes and cytoskeletal elements. Many inflammatory diseases, such as atopic dermatitis (AD) and psoriasis, are associated with barrier dysfunction. It is becoming increasingly clear that the skin barrier function is not only affected by inflammatory signals but that defects in structural components of the barrier may be the initiating event for inflammatory diseases. This view is supported by findings that mutations in filaggrin, a key structural epidermal barrier protein, cause the inflammatory skin disease AD, and that a loss of AJ components, namely epidermal p120 catenin or α-catenin results in skin inflammation.

Desmosomes have long been appreciated as intercellular junctions that are vital for maintaining the structural integrity of stratified epithelia. More recent clinical investigations of patients with diseases such as arrhythmogenic cardiomyopathy have further highlighted the importance of desmosomes in cardiac tissue, where they help to maintain coordination of cardiac myocytes. Here, we review clinical and mechanistic studies that provide insight into the functions of desmosomal proteins in skin and heart during homeostasis and in disease. While intercellular junctions are organized differently in cardiac and epithelial tissues, studies conducted in epithelial systems may inform our understanding of cardiac desmosomes. We explore traditional and non-traditional roles of desmosomal proteins, ranging from adhesive capacities to nuclear functions. Finally, we discuss how these studies can guide future investigations focused on determining the molecular mechanisms by which desmosomal mutations promote the development of cardiac diseases.