Advancing Age Alters the Contribution of Calcium Release From Smooth Endoplasmic Reticulum Stores in Superior Cervical Ganglion Cells

Behringer, Erik J.; Vanterpool, Conwin K.; Pearce, William J.; Wilson, Sean; Buchholz, John N.

doi:10.1093/gerona/gln053

Cited by 4 publications

(1 citation statement)

References 60 publications

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“…Significant to the neurotoxic potential of PCBs, RyR channel activity regulates a variety of physiological and pathophysiological processes in the central (Berridge, 2006; Dai, Hall, & Hell, 2009), and peripheral nervous systems (Behringer, Vanterpool, Pearce, Wilson, & Buchholz, 2009; Buchholz, Behringer, Pottorf, Pearce, & Vanterpool, 2007; Jackson & Thayer, 2006). Decrements in neonatal reflexes, cognitive function, motor activity, tremors, changes in autonomic functioning, and hearing impairments are consistent findings with developmental PCB exposures in studies of humans and animals, and are primarily attributed to adverse effects on the developing CNS (Darras, 2008; Fitzgerald et al, 2008; Kenet, Froemke, Schreiner, Pessah, & Merzenich, 2007; Mariussen & Fonnum, 2006; Roegge & Schantz, 2006; P.…”

Section: Dioxin-like and Non-dioxin-like Pcbsmentioning

confidence: 99%

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Pessah

Cherednichenko

Lein

2010

Pharmacology & Therapeutics

214

311

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Chronic low level polychlorinated biphenyls (PCB) exposures remain a significant public health concern since results from epidemiological studies indicate PCB burden is associated with immune system dysfunction, cardiovascular disease, and impairment of the developing nervous system. Of these various adverse health effects, developmental neurotoxicity has emerged as a particularly vulnerable endpoint in PCB toxicity. Arguably the most pervasive biological effects of PCBs could be mediated by their ability to alter the spatial and temporal fidelity of Ca 2+ signals through one or more receptor mediated processes. This review will focus on our current knowledge of the structure and function of ryanodine receptors (RyRs) in muscle and nerve cells and how PCBs and related non-coplanar structures alter these functions. The molecular and cellular mechanisms by which noncoplanar PCBs and related structures alter local and global Ca 2+ signaling properties and the possible short and long-term consequences of these perturbations on neurodevelopment and neurodegeneration are reviewed. Dioxin-like and non-dioxin-like PCBs Occurrence and concerns to public healthPolychlorinated biphenyls (PCBs) are synthetic chlorinated aromatic hydrocarbons that are non-flammable, chemically stable and have high boiling points. In the United States, PCBs were synthesized and marketed primarily as Aroclor® mixtures whose degree of chlorination was identified by a four-digit designation (e.g., 1248, 1254, 1260, etc.), with the first two digits identifying the mixture as PCBs and the last two digits identifying the percent of chlorine used during synthesis. A higher degree of PCB chlorination increases melting point and lipophilicity, whereas lower chlorination increases vapor pressure and water solubility. Similar PCB mixtures were synthesized worldwide and identified under several trade names such as Clophen® and Kanechlor®. PCB mixtures, especially those of intermediate chlorination, such as Aroclor 1248 and Aroclor 1254, were widely used in several industries for their insulation and heat dissipating properties. PCBs were also broadly incorporated into a variety of common products such as pesticide extenders, plastics, varnishes, adhesives, carbonless copy paper, newsprint, fluorescent light ballasts and caulking compounds (Ross, 2004).By 1977, when PCBs were banned, more than 600,000 tons were manufactured in the United States, and global production is estimated at over 1.5 million tons (Breivik, Sweetman, Pacyna, & Jones, 2002). Because of their extensive industrial use and chemical stability, PCBs have Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the conten...

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Section: Dioxin-like and Non-dioxin-like Pcbsmentioning

confidence: 99%

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Pessah

Cherednichenko

Lein

2010

Pharmacology & Therapeutics

214

311

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Propagation of Intracellular Ca²⁺Signals in Aged Exocrine Cells

Martín-Cano

Camello-Almaraz

Macías

et al. 2015

GERONA

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There is little information on the effects of aging in the propagation of calcium signals and its underlying mechanisms. We studied the effects of aging on propagation of Ca(2+) signals in pancreatic acinar cells. Fura-2 loaded cells isolated from young (3-4 months old) and aged (24 months old) mouse responded to acetylcholine (ACh) and cholecystokinin (CCK) with a polarized Ca(2+) response initiated at the secretory pole before spreading to the basal one. Aging slowed down the propagation of the response to ACh but enhanced the velocity of the CCK response. This pattern can be explained by the age-induced depolarization of mitochondria, because it can be reproduced in young cells by mitochondrial inhibitors. Aging also increased the role of acidic stores in the CCK signal, as judged by the folimycin-induced suppression of the polarization in aged but not in young cells. The involvement of ryanodine receptors in the ACh response was also enhanced, as indicated by the loss of polarization after the treatment with 8Br-cyclic ADP ribose. Therefore, we conclude that aging modifies differentially the propagation of ACh and CCK-evoked Ca(2+) signals through mitochondrial depolarization and changes in the role of the acidic Ca(2+) stores and ryanodine receptors in the initiation of the signals.

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Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems

Behringer

2023

American Journal of Physiology-Heart and Circulatory Physiology

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Individuals aged ≥65 years will comprise approximately 20% of the global population by 2030. Cardiovascular disease remains the leading cause of death in the world with age-related endothelial "dysfunction" as a key risk factor. As an organ in and of itself, vascular endothelium courses throughout the mammalian body to coordinate blood flow to all other organs and tissues (e.g., brain, heart, lung, skeletal muscle, gut, kidney, skin) in accord with metabolic demand. In turn, emerging evidence demonstrates that vascular aging and its co-morbidities (e.g., neurodegeneration, diabetes, hypertension, kidney disease, heart failure, and cancer) are "channelopathies" in large part. With an emphasis on distinct functional traits and common arrangements across major organs systems, the present literature review encompasses regulation of vascular ion channels that underlie blood flow control throughout the body. Regulation of myoendothelial coupling and local versus conducted signaling are discussed with new perspectives for aging and the development of chronic diseases. While equipped with an awareness of knowledge gaps in the vascular aging field, a section has been included to encompass general feasibility, role of biological sex, and additional conceptual and experimental considerations (e.g., cell regression and proliferation, gene profile analyses). The ultimate goal is for the reader to see and understand major points of deterioration in vascular function while gaining the ability to think of potential mechanistic and therapeutic strategies to sustain organ perfusion and whole-body health with aging.

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Advancing Age Alters the Contribution of Calcium Release From Smooth Endoplasmic Reticulum Stores in Superior Cervical Ganglion Cells

Cited by 4 publications

References 60 publications

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Propagation of Intracellular Ca²⁺Signals in Aged Exocrine Cells

Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems

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Advancing Age Alters the Contribution of Calcium Release From Smooth Endoplasmic Reticulum Stores in Superior Cervical Ganglion Cells

Cited by 4 publications

References 60 publications

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Minding the calcium store: Ryanodine receptor activation as a convergent mechanism of PCB toxicity

Propagation of Intracellular Ca2+Signals in Aged Exocrine Cells

Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems

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Product

Resources

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Propagation of Intracellular Ca²⁺Signals in Aged Exocrine Cells