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.
Exercise-Induced Mitochondrial Biogenesis: Molecular Regulation, Impact of Training, and Influence on Exercise Performance
Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse in The Routledge Handbook on Biochemistry of Exercise, 2020
The link between intracellular calcium levels and mitochondrial biogenesis has been demonstrated in early muscle cell experiments where induced elevations in cytosolic calcium (e.g., ionophore treatment) increased mitochondrial biogenic gene expression, mitochondrial protein content, and enzymatic activities (28, 84). Moreover, genetic ablation of the calcium-sequestering protein parvalbumin is associated with a robust increase in mitochondrial content in murine skeletal muscle, further highlighting the importance of calcium for promoting mitochondrial biogenesis (13). Calcium-induced alterations in mitochondrial phenotype are partly mediated by the calcium/calmodulin serine/threonine kinase (CaMK) (125) and protein kinase C (28). Both CaMK and the related calcium/calmodulin-dependent serine/threonine phosphatase, calcineurin (111), interact with downstream transcription factors and co-activators involved in mitochondrial biogenesis (46, 125). Similar to AMPK, calcium signalling does not seem to be required for the exercise-induced increase in mitochondrial biogenesis (29), highlighting the overlapping and multifaceted nature of contraction-induced signalling cascades in mitochondrial remodelling following exercise.
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].
Inhibitory effects of candesartan on KCa3.1 potassium channel expression and cell culture and proliferation in peripheral blood CD4+T lymphocytes in Kazakh patients with hypertension from the Xinjiang region
Published in Clinical and Experimental Hypertension, 2018
Hui Li, Jun-Ling Zhao, Yuan-Ming Zhang, Su-Xia Han
Recent studies have confirmed that a large number of EH cases are closely related to the development of inflammation, suggesting that EH is a low-grade, chronic inflammatory disease, with inflammation closely related to the occurrence and development of hypertension and damage to target organs (14–16). The expression of inflammatory factors causes the vascular inflammation and promotes the development of hypertension, which further changes the structure and function of blood vessels and causes damage to the heart, kidney, and other target organs. T-lymphocyte potassium channels have been implicated in various human disorders. The activation function of T lymphocytes, which is involved in the development of hypertension, depends on ion channels located on their cell surfaces. Studies have shown that there are four types of membrane ion channels on T lymphocytes: a voltage-gated potassium channel (Kv); a calcium-activated potassium channel (IKCal); a calcium release-activated channel (CRAC), and a volume-regulated chloride channel (Clswell). Kv and IKCal channels on lymphocytes have synergistic electrophysiological effects that maintain intracellular calcium signaling. Harrison et al. (17). demonstrated that T-lymphocyte activation and accumulation in the adventitia and perivascular adipose tissue of blood vessels are important in the pathogenesis and development of hypertension.
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