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A Phox2b BAC Transgenic Rat Line Useful for Understanding Respiratory Rhythm Generator Neural Circuitry.
Ikeda K, Takahashi M, Sato S, Igarashi H, Ishizuka T, Yawo H, Arata S, Southard-Smith EM, Kawakami K, Onimaru H
(2015) PLoS One 10: e0132475
MeSH Terms: Animals, Carbon Dioxide, Chemoreceptor Cells, Chromosomes, Artificial, Bacterial, Homeodomain Proteins, Humans, Oxygen, Pulmonary Gas Exchange, Rats, Rats, Transgenic, Respiratory Rate, Transcription Factors, Trapezoid Body
Show Abstract · Added September 28, 2015
The key role of the respiratory neural center is respiratory rhythm generation to maintain homeostasis through the control of arterial blood pCO2/pH and pO2 levels. The neuronal network responsible for respiratory rhythm generation in neonatal rat resides in the ventral side of the medulla and is composed of two groups; the parafacial respiratory group (pFRG) and the pre-Bötzinger complex group (preBötC). The pFRG partially overlaps in the retrotrapezoid nucleus (RTN), which was originally identified in adult cats and rats. Part of the pre-inspiratory (Pre-I) neurons in the RTN/pFRG serves as central chemoreceptor neurons and the CO2 sensitive Pre-I neurons express homeobox gene Phox2b. Phox2b encodes a transcription factor and is essential for the development of the sensory-motor visceral circuits. Mutations in human PHOX2B cause congenital hypoventilation syndrome, which is characterized by blunted ventilatory response to hypercapnia. Here we describe the generation of a novel transgenic (Tg) rat harboring fluorescently labeled Pre-I neurons in the RTN/pFRG. In addition, the Tg rat showed fluorescent signals in autonomic enteric neurons and carotid bodies. Because the Tg rat expresses inducible Cre recombinase in PHOX2B-positive cells during development, it is a potentially powerful tool for dissecting the entire picture of the respiratory neural network during development and for identifying the CO2/O2 sensor molecules in the adult central and peripheral nervous systems.
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13 MeSH Terms
Pancreas-specific Cre driver lines and considerations for their prudent use.
Magnuson MA, Osipovich AB
(2013) Cell Metab 18: 9-20
MeSH Terms: Animals, DNA Nucleotidyltransferases, Extracellular Matrix Proteins, Integrases, Mice, Mice, Knockout, Mice, Transgenic, Models, Animal, Pancreas, Pancreatic Hormones, Protein-Lysine 6-Oxidase, Rats, Rats, Transgenic, Recombination, Genetic, Transgenes
Show Abstract · Added August 1, 2013
Cre/LoxP has broad utility for studying the function, development, and oncogenic transformation of pancreatic cells in mice. Here we provide an overview of the Cre driver lines that are available for such studies. We discuss how variegated expression, transgene silencing, and recombination in undesired cell types have conspired to limit the performance of these lines, sometimes leading to serious experimental concerns. We also discuss preferred strategies for achieving high-fidelity driver lines and remind investigators of the continuing need for caution when interpreting results obtained from any Cre/LoxP-based experiment performed in mice.
Copyright © 2013 Elsevier Inc. All rights reserved.
2 Communities
2 Members
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15 MeSH Terms
Intermittent hypoxia and stem cell implants preserve breathing capacity in a rodent model of amyotrophic lateral sclerosis.
Nichols NL, Gowing G, Satriotomo I, Nashold LJ, Dale EA, Suzuki M, Avalos P, Mulcrone PL, McHugh J, Svendsen CN, Mitchell GS
(2013) Am J Respir Crit Care Med 187: 535-42
MeSH Terms: Amyotrophic Lateral Sclerosis, Animals, Brain-Derived Neurotrophic Factor, Glial Cell Line-Derived Neurotrophic Factor, Hypoxia, Inspiratory Capacity, Male, Motor Neurons, Phrenic Nerve, Rats, Rats, Sprague-Dawley, Rats, Transgenic, Respiratory Insufficiency, Respiratory Therapy, Stem Cell Transplantation, Superoxide Dismutase
Show Abstract · Added January 14, 2014
RATIONALE - Amyotrophic lateral sclerosis (ALS) is a devastating motor neuron disease causing paralysis and death from respiratory failure. Strategies to preserve and/or restore respiratory function are critical for successful treatment. Although breathing capacity is maintained until late in disease progression in rodent models of familial ALS (SOD1(G93A) rats and mice), reduced numbers of phrenic motor neurons and decreased phrenic nerve activity are observed. Decreased phrenic motor output suggests imminent respiratory failure.
OBJECTIVES - To preserve or restore phrenic nerve activity in SOD1(G93A) rats at disease end stage.
METHODS - SOD1(G93A) rats were injected with human neural progenitor cells (hNPCs) bracketing the phrenic motor nucleus before disease onset, or exposed to acute intermittent hypoxia (AIH) at disease end stage.
MEASUREMENTS AND MAIN RESULTS - The capacity to generate phrenic motor output in anesthetized rats at disease end stage was: (1) transiently restored by a single presentation of AIH; and (2) preserved ipsilateral to hNPC transplants made before disease onset. hNPC transplants improved ipsilateral phrenic motor neuron survival.
CONCLUSIONS - AIH-induced respiratory plasticity and stem cell therapy have complementary translational potential to treat breathing deficits in patients with ALS.
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16 MeSH Terms
Respiration and ROS production in brain and spinal cord mitochondria of transgenic rats with mutant G93a Cu/Zn-superoxide dismutase gene.
Panov A, Kubalik N, Zinchenko N, Hemendinger R, Dikalov S, Bonkovsky HL
(2011) Neurobiol Dis 44: 53-62
MeSH Terms: Animals, Blotting, Western, Brain Chemistry, Calcium, Cell Death, Demyelinating Diseases, Hydrogen Peroxide, Male, Mitochondria, Mitochondrial Membranes, Motor Neurons, Oxygen Consumption, Porins, Rats, Rats, Sprague-Dawley, Rats, Transgenic, Reactive Oxygen Species, Spinal Cord, Superoxide Dismutase
Show Abstract · Added February 17, 2016
UNLABELLED - Mitochondrial dysfunction is involved in the pathogenesis of motor neuron degeneration in the G93A mutant transgenic (tgmSOD1) animal model of ALS. However, it is unknown whether mitochondriopathy is a primary or secondary event. We isolated brain (BM) and spinal cord (SCM) mitochondria from 2 month old presymptomatic tgmSOD1 rats and studied respiration and generation of reactive oxygen species (ROS) using a new metabolic paradigm (Panov et al., Am. J. Physiol., Regul. Integr. Comp. Physiol., 2011). The yields of BM and SCM from tgmSOD1 rats were 27% and 58% lower than normal rats (WT). The rates of the State 3 and State 3U respiration of tgBM and tgSCM were normal with glutamate+pyruvate+malate as substrates but were inhibited with pyruvate+malate in tgBM and glutamate+malate in tgSCM. In tgSCM the State 4 respiration with all substrates was significantly (1.5-2 fold) increased as compared with WT-SCM. Western blot analysis showed that tgSCM had lower contents of complexes III (-60%) and IV (-35%), and the presence of mutated SOD1 protein in both tgBM and tgSCM. With glutamate+pyruvate+malate or succinate+glutamate+pyruvate+malate as substrates, tgBM and tgSCM generated 5-7 fold more ROS than normal mitochondria, and tgSCM generated two times more ROS than tgBM. We show that the major damaging ROS species in tgmSOD1 animals is H(2)O(2). It is known that mutated SOD1, damaged by H(2)O(2), associates with mitochondria, and we suggest that this further increases production of H(2)O(2). We also show that the total tissue calcium content remained normal in the brain but was diminished by 26% in the spinal cord of presymptomatic tgmSOD1 rats.
CONCLUSION - In tgSCM abnormally high rates of ROS generation, associated with reverse electron transport, result in accelerated mitochondriopathy, and the Ca(2+)-dependent excitotoxic death of motor neurons. Thus mitochondrial dysfunction is a key early element in pathogenesis of motor neuron degeneration in tgmSOD1 rats.
Copyright © 2011 Elsevier Inc. All rights reserved.
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19 MeSH Terms
Impaired-inactivation of FoxO1 contributes to glucose-mediated increases in serum very low-density lipoprotein.
Wu K, Cappel D, Martinez M, Stafford JM
(2010) Endocrinology 151: 3566-76
MeSH Terms: Adenoviridae, Animals, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Cell Nucleus, Forkhead Transcription Factors, Glucose, Glucose Clamp Technique, Hyperinsulinism, Insulin, Lipid Metabolism, Lipoproteins, VLDL, Liver, Male, Nerve Tissue Proteins, Rats, Rats, Long-Evans, Rats, Transgenic, Transduction, Genetic, Up-Regulation
Show Abstract · Added October 8, 2015
For patients with diabetes, insulin resistance and hyperglycemia both contribute to increased serum triglyceride in the form of very low-density lipoprotein (VLDL). Our objective was to define the insulin conditions in which hyperglycemia promotes increased serum VLDL in vivo. We performed hyperglycemic-hyperinsulinemic clamp studies and hyperglycemic-hypoinsulinemic clamp studies in rats, with metabolic tracers for glucose flux and de novo fatty acid synthesis. When blood glucose was clamped at hyperglycemia (17 mm) for 2 h under hyperinsulinemic conditions (4 mU/kg . min), serum VLDL levels were not increased compared with baseline. We speculated that hyperinsulinemia minimized glucose-mediated VLDL changes and performed hyperglycemic-hypoinsulinemic clamp studies in which insulin was clamped near fasting levels with somatostatin (17 mm blood glucose, 0.25 mU/kg . min insulin). Under low-insulin conditions, serum VLDL levels were increased 4.7-fold after hyperglycemia, and forkhead box O1 (FoxO1) was not excluded from the nucleus of liver cells. We tested the extent that impaired inactivation of FoxO1 by insulin was sufficient for glucose to promote increased serum VLDL. We found that, when the ability of insulin to inactivate FoxO1 is blocked after adenoviral delivery of constitutively active FoxO1, glucose increased serum VLDL triglyceride when given both by ip glucose tolerance testing (3.5-fold increase) and by a hyperglycemic clamp (4.6-fold). Under both experimental conditions in which insulin signaling to FoxO1 was impaired, we found increased activation of carbohydrate response element binding protein. These data suggest that glucose more potently promotes increased serum VLDL when insulin action is impaired, with either low insulin levels or disrupted downstream signaling to the transcription factor FoxO1.
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19 MeSH Terms