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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
The human body maintains a stable environment for its cells and tissues through a combination of physiological and biochemical processes. Cell membranes form a barrier to large molecules, allowing the cell to maintain a constant internal environment. Specific transport mechanisms are therefore required to transfer material in and out of the cell. Membranes contain many different proteins that actively or passively facilitate the movement of ions or molecules across membranes. Three major classes of transport protein are membrane channels, pumps and transporters.
Endosomal and Lysosomal Electrophysiology
Published in Bruno Gasnier, Michael X. Zhu, Ion and Molecule Transport in Lysosomes, 2020
Xiaoli Zhang, Mingxue Gu, Meiqin Hu, Yexin Yang, Haoxing Xu
Lysosomal ion channels (LICs) include those that reside primarily on LELs, e.g., TRPML1–TRPML3, TPC1–TPC2, and TMEM175, the so-called “committed” lysosomal channels, as well as plasma membrane channels that are also localized in the lysosomes, i.e., the large conductance Ca2+- and voltage-activated K+ (BK) channels and P2X4 purinergic receptors/channels, referred to as “non-committed” lysosomal channels (Figure 1.1) (Cang et al., 2015; Cang et al., 2013; Cao et al., 2015a; Cao et al., 2015b; Cheng et al., 2010; Wang et al., 2017; Wang et al., 2012; Xiong and Zhu, 2016). Lysosome-targeting trafficking motifs, e.g., double leucine (LL) motifs, are required for the highly specific expression of LICs in the lysosome (Bonifacino and Traub, 2003; Xu and Ren, 2015). Both “committed” and “non-committed” LICs, regardless of their primary locations in the cell, display significant endogenous currents in the lysosome (Xiong and Zhu, 2016). Importantly, genetic or pharmacological inhibition of the known lysosomal channels impairs lysosome function to cause lysosome storage disease (LSD)-like phenotypes in the cell (Wang et al., 2017; Xiong and Zhu, 2016; Xu and Ren, 2015).
Intercellular Communication in Three-Dimensional Culture
Published in Rolf Bjerkvig, Spheroid Culture in Cancer Research, 2017
The coordination of cell growth and differentiation as well as of tissue homeostasis and synchronization of tissue functions requires the transfer of information between cells. This may be achieved by an unidirectional signal flow, as is the case with secreted molecules (hormones, neurotransmitters) and/or with membrane-bound receptors (sperm-egg binding, immune system). It can also follow a “nonrectifying” mode, as is observed for direct intercellular communication via gap junctions that are formed in regions of close cell-to-cell contact. These membrane channels are not only bidirectionally permeable and facilitate the free exchange of charged and neutral molecules, but also connect adjacent cells mechanically. They must be clearly discriminated from desmosomes, which anchor cells together to form structural or functional units, as well as from tight junctions that seal membranes of epithelial cells to each other so that the paracellular path becomes impermeable to molecules, and a polarity of apical and basolateral surface is maintained.
An overview of carbonic anhydrases and membrane channels of synoviocytes in inflamed joints
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Currently, experimental evidence for the involvement of CAs and FLS membrane channels in RA is limited. The physiological and pathological roles of ion channels and transporters in dynamic FLS migration have not yet been studied in detail. Here, we have summarised the studies on membrane channels and regulatory enzymes of RA-FLS with an aim to understand their migrated state. However, many questions regarding RA-FLS still need to be clarified. What are the exact molecular mechanisms by which ion transporter affects the FLS migration apparatus? What are the exact components of synovial fluid that mediate the FLS dynamics? What are the components affecting the differential expression of CAs and membrane channels in FLS? What is the combined mechanism of CAs as regulatory enzymes? Several membrane channels and transporters show tissue-specific expression. Thus, unravelling the mechanisms by which ion channels and transporters are positioned in and modulate the migration of activated FLS will be a rewarding pursuit for the coming years. The motivation of channel physiologists is also needed to develop potential therapeutics to counter the critical pathophysiological involvement of FLS migration in joints in RA.
Resonant interaction between electromagnetic fields and proteins: A possible starting point for the treatment of cancer
Published in Electromagnetic Biology and Medicine, 2018
Emanuele Calabrò, Salvatore Magazù
Despite different values between normal and cancerous cells were found in these studies, such models are based only on mechanical properties of cells, which, in our opinion, cannot be applied to detect representative natural frequencies of cancer cells. Indeed, the more complicated the organism, the more frequency involved, because cells are made up of billions of molecules each having its resonant frequency, so that a unique resonant frequency of a cell cannot be easily found. Hence, in order to highlight a resonance between cancerous cells and an applied EMF aimed to damage such cells, the most important physical chemical mechanism in the cellular functions should be taken into account. This mechanism is the alteration of ions’ flux across cellular membrane channels that can be induced by the displacement of proteins’ α-helices exposed to EMFs. Indeed cellular functions strictly depends on the flux of ions across cellular membrane channels. In the following sections, it is explained how this mechanism could be applied to cancer treatment.
Preservation of neuronal function as measured by clinical and MRI endpoints in relapsing-remitting multiple sclerosis: how effective are current treatment strategies?
Published in Expert Review of Neurotherapeutics, 2018
Christiane Graetz, Sergiu Groppa, Frauke Zipp, Nelly Siller
As far as the pathophysiology is concerned, it does not seem to be necessary to choose between an inflammatory or a neurodegenerative cause for MS risk and disability. Instead, it is plausible to unify these concepts by observing both immune and neurodegenerative processes from the beginning, but with varying importance over the course of disease. Immunity, energy failure, and membrane channel dysfunction may all be key processes in progressive disease, as reviewed by [12]. MS is believed to be caused by the interplay of genetic variants and environmental influences [13–17]. Interestingly, RRMS and PPMS show no differences in susceptibility variants; therefore, the dissimilarities in clinical course might be influenced by other genetic variants or environmental factors [18].