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Cell structure, function and adaptation
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Cells are joined by several types of cell junction that are physical connections. Desmosomes and tight junctions join cell membranes, and gap junctions allow passage of chemical messages between cells. In addition, adhesion molecules are expressed on cell surfaces, not only joining cells together but also transducing signals important for growth, migration, and differentiation. The surface-bound major histocompatibility complex (MHC) molecules and immunoglobulin are specialized forms of recognition mechanism present in lymphocytes, without which an immune response would be impossible.
Cardiac and cardiovascular disorders
Published in Angus Clarke, Alex Murray, Julian Sampson, Harper's Practical Genetic Counselling, 2019
In ARVC, the cardiac muscle is replaced by fibrosis and fat, in the right ventricle more than the left. The genes implicated are important for the integrity of cell-cell junctions, such as plakophilin-2 (PKP-2). The condition is characterised by ECG abnormalities, dysrhythmias and sometimes heart failure. Changes may also be seen on cardiac echo. ARVC may lead to sudden death. Specialist cardiac pathology may be required to identify the disorder at examination postmortem. Treatment can be difficult and may require transplantation.
Notes on Cancer
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
Normal cells in culture proliferate only to a set limit, i.e., crowding stops mitosis.341 The implication from many studies along this line is that cells communicate with each other. Normal cells in tissue culture will not tolerate a free edge; they grow until the edge of the culture contacts a surface.358 Such cells growing in culture continue proliferation until they make intercellular contact.359 Cell junctions form with the tendency to remain a monolayer. This process has been termed “contact inhibition”. It is seen with the growth of epidermis closing over a skin wound.360 When the free edges meet, there is an abrupt cessation of growth. Contact inhibition crosses the species barrier.361 Normal human cells exhibit this tendency.362
Desmosomes undergo dynamic architectural changes during assembly and maturation
Published in Tissue Barriers, 2022
Reena R. Beggs, Tejeshwar C. Rao, William F. Dean, Andrew P. Kowalczyk, Alexa L. Mattheyses
Considering our data in the context of other epithelial junctions, we note that tight junctions and gap junctions are also known to undergo structural remodeling, although the underlying mechanisms have not been fully elucidated.37,38 The interplay between different cell junctions is complex, and junctions are historically studied in isolation, which makes investigating interactions between different cell junctions difficult.39 Signaling and colocalization have been previously implicated in communication between some junctions. One possible way that desmosomes could impact other junctions is through an interaction between desmoplakin and microtubule binding proteins.40,41 This has been demonstrated by a mutation in desmoplakin, which leads to aberrant targeting of gap junction proteins as a result of misregulation of microtubule dynamics.42 It is possible interactions with microtubule binding proteins that could be transmitted through architectural changes. The nature of junction architecture in different tissue types, and possible implications of architectural interactions between junctions, is a largely unexplored area with potential for great importance in understanding cell adhesion and communication.
Cell-cell junctions: structure and regulation in physiology and pathology
Published in Tissue Barriers, 2021
Mir S. Adil, S. Priya Narayanan, Payaningal R. Somanath
Intercellular junctions are structurally and biochemically differentiated regions of the plasma membrane through which adjacent cells interact in a specific manner. These structures were originally identified and named according to their morphology and purported function.29 To retain barrier function and to prevent the invasion of pathogens and their rapid systemic spread, cell junctions need to be kept tight and repaired quickly after vessel rupture.30 There are three functional categories of cell junction: anchoring junctions; tight, or occluding, junctions, and gap (GJ), or permeable, junctions Figure 1.17,31,32 The AJs and desmosomes provide essential adhesive and mechanical properties that contribute to barrier function but do not seal the paracellular space,33 the TJs hold cells together and form a near leakproof intercellular seal by fusion of adjacent cell membranes34 since interactions between cells are important for the assembly and maintenance of three-dimensional tissues.35 The latter is a selectively permeable barrier that generally represents the rate-limiting step of paracellular transport.33 Many cell types also possess GJs, which allow small molecules to pass from one cell to the next through channels.34
An overview on natural farnesyltransferase inhibitors for efficient cancer therapy
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2020
Xiaohan Dai, Yingni Sun, Ting Zhang, Yongfei Ming, Gao Hongwei
Tumour refers to the local mass formed by abnormal proliferation of local tissue under the action of various tumorigenic factors. It is one of the world’s five terminally ill diseases including motor neuron disease, AIDS, leukaemia, and rheumatoid arthritis. Cancer cells have unique properties of invasion and metastasis. Tumours disrupt cell junctions and cell signalling, leading to important gene dysfunction1. At present, the main methods for treating tumours are still traditional treatments such as surgical treatment, chemotherapy, and radiation therapy, which usually have strong toxic side effects and are prone to drug resistance. With the development of related disciplines such as molecular biology, research on anti-tumour drugs has also shifted to new anti-tumour drugs targeting multiple links in the mechanism of tumour development. These drugs, for example, targeting cell signalling molecules: including protein tyrosine kinase inhibitors, farnesyltransferase inhibitors (FTIs), mitogen-activated protein kinase (MAPK) signalling pathway inhibitors, cell cycle regulators, etc., are localised to target cell-specific bio-macromolecules, thereby inhibiting the growth and metastasis of tumour cells, rather than killing cells directly. Among them, FTIs are one of the hotspots in recent years, which have attracted the attention of many famous research institutions at home and abroad.