Mitochondria and Embryo Viability
Carlos Simón, Carmen Rubio in Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
The best understood mitochondrial functions include ATP production by oxidative phosphorylation, β-oxidation of fatty acids, and metabolism of amino acids and lipids. (11). Mitochondria also have other complex functions, including participating in a variety of cell-signaling cascades. Proteins such as GTPases, kinases, and phosphatases facilitate bidirectional communication between the mitochondria and the rest of the cell, helping to regulate metabolism, cell cycle control, development, and antiviral responses (12). A key example of the mitochondria's integration in signaling pathways is its role in the apoptotic cascade (13), with mitochondrial fragmentation and cristae remodeling being essential steps for cytochrome c release and cell death (12). Additionally, calcium signaling causes a dynamic change in the phosphorylation state of numerous proteins (14). Mitochondria act both as a calcium buffer and as the propagator of intracellular calcium waves during muscle contraction and synaptic vesicle release (12). Another example of the integration of mitochondria in signaling pathways is its role in the apoptotic cascade and cell death (13); indeed, mitochondrial fragmentation and cristae remodeling are essential steps for “cytochrome c” release and cell death (12).
Assessment of Second Messenger Function in the Hippocampus of Aged Rats with Cognitive Impairment
David R. Riddle in Brain Aging, 2007
Studies in behaviorally characterized aged rat have demonstrated that decrements in muscarinic and metabotropic glutamate receptor function in the hippocampus are related to cognitive impairment. Alterations in signal transduction have been observed as far upstream as receptor/G-protein coupling and as far downstream as PI turnover, although the molecular machinery, measured by Western blotting and receptor autoradiography, remains intact. Receptor-mediated Gαq/11 signaling ultimately influences intracellular calcium levels, via the IP3 receptors on the endoplasmic reticulum or via protein kinase C and interaction with cell membrane calcium channels. Regulation of calcium signaling has far-reaching consequences, from modulation of synaptic plasticity to cellular toxicity. Our recent data indicating that age-related alterations in receptor signaling occur very early in the cascade at the level of the G-protein suggest that receptor/G-protein coupling is a mechanism to consider for repair and/or protection in the aged brain.
Mitochondrial Dysfunction in Chronic Kidney Disease
Shamim I. Ahmad in Handbook of Mitochondrial Dysfunction, 2019
The polycystins, PC1 (Hughes et al. 1995) and PC2 (Hayashi et al. 1997), protein products of PKD1 and PKD2 respectively (Kottgen 2007), localize principally to the plasma membranes of the primary cilia, but also in a number of other locations such as the endoplasmic reticulum (ER) (likely a major site of PC2). PC1 participates in cell-cell and cell-matrix interactions, whereas PC2 is a non-selective cation channel with great permeability to calcium (Cai et al. 1999). PC1 and PC2 interact with several proteins involved in calcium signaling, including inositol 1,4,5-trisphosphate receptor (Li et al. 2005, 2009; Santoso et al. 2011), ryanodine-2 (Anyatonwu et al. 2007), and others (Kottgen et al. 2008; Tsiokas et al. 1999), modulating calcium release from intracellular deposits (Nauli et al. 2003, 2006). PC1 and PC2 dysfunction activates calcium-sensitive adenylyl cyclases, increasing cyclic adenosine monophosphate (cAMP) (Torres and Harris 2014b). This in turn activates several pathways that modulate cell migration, differentiation, proliferation, and apoptosis, including the mammalian target of rapamycin (mTOR) and extracellular-signal-regulated kinases (ERK).
Red-light radiation: does it enhance memory by increasing hippocampal LRP-1 and TRPA-1 genes expression?
Published in International Journal of Radiation Biology, 2023
Saereh Haghjoo, Mojtaba Hedayati Ch, Mohammad Rostampour, Behrooz Khakpour-Taleghani
Normal intracellular calcium signaling appears to be an essential factor in neuronal survival and AD pathogenesis. Transient receptor potential ankyrin-1 (TRPA-1) is a neuronal calcium channel which has known as the sensor of several parameters, including ROS (Lee et al. 2016; Schampel and Kuerten 2017). TRPA-1 plays an important regulatory role in mitochondrial dysfunction, calcium homeostasis, physiological function of astrocytes, and inflammatory responses which involve in neurodegenerative diseases (ND) (Borbély et al. 2019). It has been hypothesized that an increase in intracellular calcium, due to Aβ accumulation, may be the cause of neuronal destruction in AD (Tong et al. 2018). TRPA-1 is also a critical factor in regulating the inflammatory responses to a few stimuli such as bacterial endotoxin, LPS (Borbély et al. 2019). It has also been shown that cooperating of TRP and NMDA receptors, similar to glutamate receptors in the hippocampus CA1 region, is essential for synaptogenesis, synaptic plasticity, and memory enhancement (You et al. 2020).
Toxoplasma gondii infection and risk of attention-deficit hyperactivity disorder: a systematic review and meta-analysis
Published in Pathogens and Global Health, 2020
Tooran Nayeri, Shahabeddin Sarvi, Mahmood Moosazadeh, Zahra Hosseininejad, Afsaneh Amouei, Ahmad Daryani
T. gondii affects the expression of approximately 3000 host genes throughout its life cycle. Susceptibility genes for mental disorders, such as ADHD, are highly enriched in the human arm of this interactome. Moreover, the expression of 17.7% of 237 ADHD susceptibility genes is affected by the Toxoplasma infection [55,56]. Furthermore, the primary common emphasis in ADHD was on the calcium-signaling pathway and number of other metabolic pathways, such as tyrosine, tryptophan, and histidine, and the number of recovered genes in this pathway is 44 [55,57]. The calcium-signaling pathway is activated by voltage or receptor-gated ion channels, processes modulating intracellular stores, and phosphatidylinositol signaling system [58]. Calcium channel blockers, calmodulin antagonism, or extracellular calcium reduce cell invasion by parasites [59,60].
Effects of potassium channel knockdown on peripheral blood T lymphocytes and NFAT signaling pathway in Xinjiang Kazak patients with hypertension
Published in Clinical and Experimental Hypertension, 2023
Chen Dai, Meng Tan, Xiaopan Meng, Jian Dong, Yuanming Zhang
Previous studies have demonstrated that the potassium channels and nuclear factor of activated T cells (NFAT) are closely related to the T lymphocyte activation (17,18). There are two major types of membrane ion channels on T lymphocytes, namely the voltage-gated potassium channels (Kv1.3) and calcium-activated potassium channels (KCa3.1) (19). These channels help maintain membrane potential by mediating the outflow of potassium, while the altered membrane potential would indirectly affect the calcium signaling within the cells (20). Therefore, the potassium channels on T lymphocytes are closely related to the intracellular Ca2+ regulation. Calcium is an important second messenger associated with the NFAT signaling pathway. Increased Ca2+ concentration can activate the calcineurin (CaN), which triggers the T lymphocyte activation through NFAT signaling pathway (21) 1. The NFAT signaling pathway can also mediate the lymphocyte proliferation and differentiation. Furthermore, NFAT would activate the production of cytokines, including the tumor necrosis factor-α, IL-4, IL-6, and IFN-β (22). Whether the potassium channels are involved in the occurrence of inflammatory state in the body through the NFAT signaling pathway remains to be elucidated.
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