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Mitochondria and Embryo Viability
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Irene Corachan Garcia, Laura Iñiguez Quiles, Antonio Diez-Juan
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).
Role of Vitamin D and Antioxidants in the Prevention and Treatment of Alzheimer’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Shilia Jacob Kurian, Ruby Benson, Sonal Sekhar Miraj, Mahadev Rao
Dysregulation in intracellular calcium signaling is widely implicated in the pathophysiology of AD, which results in lesions, hyperphosphorylation of tau, and finally neurodegeneration. Mitochondrial activities largely depend on calcium from the endoplasmic reticulum (ER) or extracellular space. Inositol 1,4,5-trisphosphate (IP3) is the second messenger and the inositol 1,4,5-trisphosphate receptors (IP3Rs) are intracellular ion channels, which stimulate the release of calcium from the ER (Bizzarri et al. 2016; Egorova and Bezprozvanny 2018).
Exercise-Induced Mitochondrial Biogenesis: Molecular Regulation, Impact of Training, and Influence on Exercise Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Hashim Islam, Jacob T. Bonafiglia, Cesare Granata, Brendon J. Gurd
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).
World Trade Center dust induces nasal and neurological tissue injury while propagating reduced olfaction capabilities and increased anxiety behaviors
Published in Inhalation Toxicology, 2022
Michelle Hernandez, Joshua Vaughan, Terry Gordon, Morton Lippmann, Sam Gandy, Lung-Chi Chen
Dysregulation of intracellular calcium homeostasis or aberrant calcium signaling has been implicated in CNS dysfunction, affecting both neuronal and non-neuronal cells (Chakroborty and Stutzmann 2011; Magi et al. 2016). Aspartate Beta-Hydroxylase (Asph) gene involvement in calcium homeostasis has been greatly detailed throughout molecular literature but has not been extensively researched in the exposure sciences (Dinchuk et al. 2000; Yang et al. 2010). Preliminary evidence for calcium dysregulation has been presented with Asph mRNA transcript upregulation (15–20%) 90-days post-exposure in mice (Supplemental Figure 5). Equally, oxidative stress had also been implicated in early AD pathologies, linked to metal homeostatic imbalances (Miranda et al. 2000; Bayer et al. 2006). Despite unremarkable SOD2 mRNA transcripts at 90 days post-WTCPM exposure, SOD2 data are informative in terms of functional pathogenesis with respect to neurological disease manifestations. SOD2 is a major mitochondrial antioxidant defense enzyme involved in free radical detoxification with critical implications regarding calcium homeostasis maintenance in neuronal cells (Zhao et al. 2019).
Deciphering Alzheimer’s disease: predicting new therapeutic strategies via improved understanding of biology and pathogenesis
Published in Expert Opinion on Therapeutic Targets, 2020
Rita Khoury, George T. Grossberg
Astrocytes are star-shaped cells that constitute the most abundant type of glial cells in the brain outnumbering neurons by about five-fold [29]. They are responsible for synaptic activity modulation and glutamate homeostasis, blood-brain barrier (BBB) formation and inflammatory response [30]. They also play a critical role in the repair and scarring process following all forms of brain insults/injuries through a process called reactive astrogliosis and glial scar formation [29]. It is believed that astrocytic dysfunction promotes secretases’ activity leading to overproduction of Aβ deposits and impaired clearance of these plaques through the BBB once formed. Progressive accumulation of the plaques will trigger by itself further astrocytic activation/dysfunction yielding a vicious circle between amyloidosis and astrocytic activation [31]. Furthermore, intracellular calcium signaling is crucial to neuronal function, synaptic transmission and plasticity mechanisms underlying learning and memory [32]. Secretion of inflammatory mediators such as bradykinin stimulates the release of intracellular calcium and increased glutamate leading to excitotoxicity [33]. An association between reactive astrocytes and neurofibrillary tangle formation has also been shown in AD postmortem neuropathological studies, although it is less studied compared to the senile plaques [30].