scholarly journals Ontogeny of Carbon Monoxide-Related Gene Expression in a Deep-Diving Marine Mammal

2021 ◽  
Vol 12 ◽  
Author(s):  
Elizabeth R. Piotrowski ◽  
Michael S. Tift ◽  
Daniel E. Crocker ◽  
Anna B. Pearson ◽  
José P. Vázquez-Medina ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Carbon Monoxide ◽  
Mitochondrial Biogenesis ◽  
Oxygen Storage ◽  
Antioxidant Defenses ◽  
Deep Diving ◽  
Immune System Activation ◽  
Expression Of Genes

Marine mammals such as northern elephant seals (NES) routinely experience hypoxemia and ischemia-reperfusion events to many tissues during deep dives with no apparent adverse effects. Adaptations to diving include increased antioxidants and elevated oxygen storage capacity associated with high hemoprotein content in blood and muscle. The natural turnover of heme by heme oxygenase enzymes (encoded by HMOX1 and HMOX2) produces endogenous carbon monoxide (CO), which is present at high levels in NES blood and has been shown to have cytoprotective effects in laboratory systems exposed to hypoxia. To understand how pathways associated with endogenous CO production and signaling change across ontogeny in diving mammals, we measured muscle CO and baseline expression of 17 CO-related genes in skeletal muscle and whole blood of three age classes of NES. Muscle CO levels approached those of animals exposed to high exogenous CO, increased with age, and were significantly correlated with gene expression levels. Muscle expression of genes associated with CO production and antioxidant defenses (HMOX1, BVR, GPX3, PRDX1) increased with age and was highest in adult females, while that of genes associated with protection from lipid peroxidation (GPX4, PRDX6, PRDX1, SIRT1) was highest in adult males. In contrast, muscle expression of mitochondrial biogenesis regulators (PGC1A, ESRRA, ESRRG) was highest in pups, while genes associated with inflammation (HMOX2, NRF2, IL1B) did not vary with age or sex. Blood expression of genes involved in regulation of inflammation (IL1B, NRF2, BVR, IL10) was highest in pups, while HMOX1, HMOX2 and pro-inflammatory markers (TLR4, CCL4, PRDX1, TNFA) did not vary with age. We propose that ontogenetic upregulation of baseline HMOX1 expression in skeletal muscle of NES may, in part, underlie increases in CO levels and expression of genes encoding antioxidant enzymes. HMOX2, in turn, may play a role in regulating inflammation related to ischemia and reperfusion in muscle and circulating immune cells. Our data suggest putative ontogenetic mechanisms that may enable phocid pups to transition to a deep-diving lifestyle, including high baseline expression of genes associated with mitochondrial biogenesis and immune system activation during postnatal development and increased expression of genes associated with protection from lipid peroxidation in adulthood.

Regulation of skeletal muscle mitochondrial function by nuclear receptors: implications for health and disease

2015 ◽  
Vol 129 (7) ◽  
pp. 589-599 ◽  
Author(s):  
Joaquin Perez-Schindler ◽  
Andrew Philp
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Nuclear Receptors ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Metabolic Diseases ◽  
Therapeutic Potential ◽  
Muscle Metabolism ◽  
Cellular Level ◽  
Expression Of Genes

Skeletal muscle metabolism is highly dependent on mitochondrial function, with impaired mitochondrial biogenesis associated with the development of metabolic diseases such as insulin resistance and type 2 diabetes. Mitochondria display substantial plasticity in skeletal muscle, and are highly sensitive to levels of physical activity. It is thought that physical activity promotes mitochondrial biogenesis in skeletal muscle through increased expression of genes encoded in both the nuclear and the mitochondrial genome; however, how this process is co-ordinated at the cellular level is poorly understood. Nuclear receptors (NRs) are key signalling proteins capable of integrating environmental factors and mitochondrial function, thereby providing a potential link between exercise and mitochondrial biogenesis. The aim of this review is to highlight the function of NRs in skeletal muscle mitochondrial biogenesis and discuss the therapeutic potential of NRs for the management and treatment of chronic metabolic disease.

scholarly journals The Language of Reactive Oxygen Species Signaling in Plants

2012 ◽  
Vol 2012 ◽  
pp. 1-22 ◽  
Author(s):  
Soumen Bhattacharjee
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Lipid Peroxidation ◽  
Reactive Oxygen ◽  
Environmental Cues ◽  
Oxygen Species ◽  
Lipid Peroxidation Products ◽  
Expression Of Genes ◽  
Regulated Gene Expression

Reactive oxygen species (ROS) are astonishingly versatile molecular species and radicals that are poised at the core of a sophisticated network of signaling pathways of plants and act as core regulator of cell physiology and cellular responses to environment. ROS are continuously generated in plants as an inevitable consequence of redox cascades of aerobic metabolism. In one hand, plants are surfeited with the mechanism to combat reactive oxygen species, in other circumstances, plants appear to purposefully generate (oxidative burst) and exploit ROS or ROS-induced secondary breakdown products for the regulation of almost every aspect of plant biology, from perception of environmental cues to gene expression. The molecular language associated with ROS-mediated signal transduction, leading to modulation in gene expression to be one of the specific early stress response in the acclamatory performance of the plant. They may even act as “second messenger” modulating the activities of specific proteins or expression of genes by changing redox balance of the cell. The network of redox signals orchestrates metabolism for regulating energy production to utilization, interfering with primary signaling agents (hormones) to respond to changing environmental cues at every stage of plant development. The oxidative lipid peroxidation products and the resulting generated products thereof (associated with stress and senescence) also represent “biological signals,” which do not require preceding activation of genes. Unlike ROS-induced expression of genes, these lipid peroxidation products produce nonspecific response to a large variety of environmental stresses. The present review explores the specific and nonspecific signaling language of reactive oxygen species in plant acclamatory defense processes, controlled cell death, and development. Special emphasis is given to ROS and redox-regulated gene expression and the role of redox-sensitive proteins in signal transduction event. It also describes the emerging complexity of apparently contradictory roles that ROS play in cellular physiology to ascertain their position in the life of the plant.

Relationship between anoxia exposure and antioxidant status in the frog Rana pipiens

1996 ◽  
Vol 271 (4) ◽  
pp. R918-R925 ◽  
Author(s):  
M. Hermes-Lima ◽  
K. B. Storey
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Rana Pipiens ◽  
Thiobarbituric Acid ◽  
Leopard Frog ◽  
Antioxidant Defenses ◽  
Glutathione S Transferase ◽  
Glutathione Status ◽  
Organ Specific

The biochemical adaptations of cellular antioxidant defenses that permit anoxia-tolerant animals to deal effectively with rapid and large changes in oxygen availability, and hence oxidative stress, during transitions from anoxia to normoxia provide insights into the strategies of antioxidant defense that could help to minimize reperfusion injuries to mammalian organs after anoxia/ischemia stress. The present study analyzes the effects of 30 h anoxia exposure followed by reoxygenation on the antioxidant defenses (activities of five enzymes, glutathione status) and lipid peroxidation damage to organs of the leopard frog Rana pipiens (5 degrees C-adapted autumn frogs). Exposure to 30 h anoxia resulted in significant increases in the activities of skeletal muscle and heart catalase (by 53 and 47%), heart and brain glutathione peroxidase (by 75 and 30%), and brain glutathione S-transferase (by 66%). In most cases, enzyme activities had returned to the control values after 40 h aerobic recovery. Activities of superoxide dismutase and glutathione reductase were unaltered in all of the organs, and anoxia/recovery had no effect on any of the enzymes in liver. Glutathione equivalents (GSH-eq) were maintained in four organs during anoxia but decreased by 32% in brain during anoxia. Brain GSH-eq had recovered after 90 min reoxygenation, and, in addition, hepatic GSH-eq rose by 71% after 90 min reoxygenation. The ratio of oxidized glutathione to GSH-eq was also affected by anoxia in an organ-specific way. Lipid peroxidation, assessed as the content of thiobarbituric acid-reactive substances (TBARS), was unaltered in skeletal muscle and liver after 30 h anoxia exposure or short (25 and 90 min)- or long-term (40 h) periods of reoxygenation, indicating that cycles of natural and survivable anoxia/reoxygenation occur without significant increase in TBARS in selected organs. Overall, the data demonstrate that elements of the antioxidant system of R. pipiens are induced during anoxia exposures as a possible preparation for dealing with potentially harmful oxygen reperfusion stress.

scholarly journals Monolluma quadrangulaProtects against Oxidative Stress and Modulates LDL Receptor and Fatty Acid Synthase Gene Expression in Hypercholesterolemic Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
May N. Bin-Jumah
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lipid Peroxidation ◽  
Fatty Acid ◽  
Proinflammatory Cytokines ◽  
Fatty Acid Synthase ◽  
Heart Function ◽  
Ldl Receptor ◽  
Antioxidant Defenses ◽  
Creatine Kinase Mb

Hypercholesterolemia is a metabolic disorder associated with oxidative stress. The present study investigated the protective effect ofMonolluma quadrangulaextract on hypercholesterolemia-induced oxidative stress in the liver and heart of high-cholesterol-diet- (HCD-) fed rats. The experimental animals received HCD for 10 weeks and were concurrently treated with 300 or 600 mg/kgM. quadrangulaextract. HCD-fed rats showed a significant increase in serum triglycerides, total cholesterol, LDL-cholesterol, vLDL-cholesterol, and cardiovascular risk indices along with decreased HDL-cholesterol and antiatherogenic index. TheM. quadrangulaextract significantly improved dyslipidemia and atherogenesis in HCD-fed rats. HCD induced a significant increase in serum transaminases, creatine kinase-MB, and proinflammatory cytokines. In addition, HDC induced a significant increase in hepatic and cardiac lipid peroxidation and decreased antioxidant enzymes. Treatment with theM. quadrangulaextract significantly alleviated liver and heart function markers, decreased proinflammatory cytokines and lipid peroxidation, and enhanced the antioxidant defenses. Also, theM. quadrangulaextract significantly reduced the expression of fatty acid synthase (FAS) and increased the expression of LDL receptor in the liver of HCD-fed rats. In conclusion, theM. quadrangulaextract has a potent antihyperlipidemic and cholesterol-lowering effect on HCD-fed rats. The beneficial effects of theM. quadrangulaextract were mediated through the increased antioxidant defenses, decreased inflammation and lipid peroxidation, and modulated hepatic FAS and LDL receptor gene expression.

scholarly journals Chronic Alcohol Dysregulates Skeletal Muscle Myogenic Gene Expression after Hind Limb Immobilization in Female Rats

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 441
Author(s):  
Danielle E. Levitt ◽  
Alice Y. Yeh ◽  
Matthew J. Prendergast ◽  
Ronald G. Budnar, Jr. ◽  
Katherine A. Adler ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Hind Limb ◽  
Female Rats ◽  
Skeletal Muscle Regeneration ◽  
Skeletal Muscle Atrophy ◽  
Expression Of Genes ◽  
Risk Factors For Falls ◽  
Limb Immobilization

Alcohol use and aging are risk factors for falls requiring immobilization and leading to skeletal muscle atrophy. Skeletal muscle regeneration is integral to post-immobilization recovery. This study aimed to elucidate the effects of alcohol and ovarian hormone loss on the expression of genes implicated in muscle regeneration. Three-month-old female rats received an ovariectomy or a sham surgery, consumed an alcohol-containing or control diet for 10 weeks, were subjected to unilateral hind limb immobilization for seven days, and finally were allowed a three (3d)- or 14 (14d)-day recovery. Immobilization decreased the quadriceps weight at 3d and 14d, and alcohol decreased the quadriceps weight at 14d in the nonimmobilized hind limb (NI). At 3d, alcohol decreased gene expression of myoblast determination protein (MyoD) in the immobilized hind limb (IMM) and myocyte enhancer factor (Mef)2C and tumor necrosis factor (TNF)α in NI, and ovariectomy increased MyoD and decreased TNFα expression in NI. At 14d, alcohol increased the gene expression of Mef2C, MyoD, TNFα, and transforming growth factor (TFG)β in IMM and decreased monocyte chemoattractant protein (MCP)1 expression in NI; ovariectomy increased TNFα expression in NI, and alcohol and ovariectomy together increased Mef2C expression in NI. Despite increased TGFβ expression, there was no concomitant alcohol-mediated increase in collagen in IMM at 14d. Overall, these data indicate that alcohol dysregulated the post-immobilization alteration in the expression of genes implicated in regeneration. Whether alcohol-mediated molecular changes correspond with post-immobilization functional alterations remains to be determined.

scholarly journals Hypothalamic malonyl-CoA triggers mitochondrial biogenesis and oxidative gene expression in skeletal muscle: Role of PGC-1 

2006 ◽  
Vol 103 (42) ◽  
pp. 15410-15415 ◽  
Author(s):  
S.-H. Cha ◽  
J. T. Rodgers ◽  
P. Puigserver ◽  
S. Chohnan ◽  
M. D. Lane
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Malonyl Coa

scholarly journals Impact of hot and cold exposure on human skeletal muscle gene expression

2017 ◽  
Vol 42 (3) ◽  
pp. 319-325 ◽  
Author(s):  
Roksana B. Zak ◽  
Robert J. Shute ◽  
Matthew W.S. Heesch ◽  
D. Taylor La Salle ◽  
Matthew P. Bubak ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Room Temperature ◽  
Environmental Temperature ◽  
Human Model ◽  
Whole Body ◽  
Muscle Gene Expression ◽  
Muscle Gene ◽  
The Impact

Many human diseases lead to a loss of skeletal muscle metabolic function and mass. Local and environmental temperature can modulate the exercise-stimulated response of several genes involved in mitochondrial biogenesis and skeletal muscle function in a human model. However, the impact of environmental temperature, independent of exercise, has not been addressed in a human model. Thus, the purpose of this study was to compare the effects of exposure to hot, cold, and room temperature conditions on skeletal muscle gene expression related to mitochondrial biogenesis and muscle mass. Recreationally trained male subjects (n = 12) had muscle biopsies taken from the vastus lateralis before and after 3 h of exposure to hot (33 °C), cold (7 °C), or room temperature (20 °C) conditions. Temperature had no effect on most of the genes related to mitochondrial biogenesis, myogenesis, or proteolysis (p > 0.05). Core temperature was significantly higher in hot and cold environments compared with room temperature (37.2 ± 0.1 °C, p = 0.001; 37.1 ± 0.1 °C, p = 0.013; 36.9 ± 0.1 °C, respectively). Whole-body oxygen consumption was also significantly higher in hot and cold compared with room temperature (0.38 ± 0.01 L·min−1, p < 0.001; 0.52 ± 0.03 L·min−1, p < 0.001; 0.35 ± 0.01 L·min−1, respectively). In conclusion, these data show that acute temperature exposure alone does not elicit significant changes in skeletal muscle gene expression. When considered in conjunction with previous research, exercise appears to be a necessary component to observe gene expression alterations between different environmental temperatures in humans.

scholarly journals The role of calcium and calcium/calmodulin-dependent kinases in skeletal muscle plasticity and mitochondrial biogenesis

2004 ◽  
Vol 63 (2) ◽  
pp. 279-286 ◽  
Author(s):  
Eva R. Chin
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Activated T Cells ◽  
Muscle Plasticity ◽  
Hypertrophic Growth ◽  
Muscle Gene Expression ◽  
Calcium Calmodulin Dependent ◽  
Biological Phenomena ◽  
Expression Of Genes ◽  
Muscle Gene

Intracellular Ca2+plays an important role in skeletal muscle excitation–contraction coupling and also in excitation–transcription coupling. Activity-dependent alterations in muscle gene expression as a result of increased load (i.e. resistance or endurance training) or decreased activity (i.e. immobilization or injury) are tightly linked to the level of muscle excitation. Differential expression of genes in slow- and fast-twitch fibres is also dependent on fibre activation. Both these biological phenomena are, therefore, tightly linked to the amplitude and duration of the Ca2+transient, a signal decoded downstream by Ca2+-dependent transcriptional pathways. Evidence is mounting that the calcineurin–nuclear factor of activated T-cells pathway and the Ca2+/calmodulin-dependent kinases (CaMK) II and IV play important roles in regulating oxidative enzyme expression, mitochondrial biogenesis and expression of fibre-type specific myofibrillar proteins. CaMKII is known to decode frequency-dependent information and is activated during hypertrophic growth and endurance adaptations. Thus, it was hypothesized that CaMKII, and possibly CaMKIV, are down regulated during muscle atrophy and levels of expression of CaMKIIα, -IIβ, -IIγ and -IV were assessed in skeletal muscles from young, aged and denervated rats. The results indicate that CaMKIIγ, but not CaMKIIα or -β, is up regulated in aged and denervated soleus muscle and that CaMKIV is absent in skeletal but not cardiac muscle. Whether CaMKIIγ up-regulation is part of the pathology of wasting or a result of some adaptational response to atrophy is not known. Future studies will be important in determining whether insights from the adaptational response of muscle to increased loads will provide pharmacological approaches for increasing muscle strength or endurance to counter muscle wasting.

scholarly journals Resistance exercise training influences skeletal muscle immune activation: a microarray analysis

2012 ◽  
Vol 112 (3) ◽  
pp. 443-453 ◽  
Author(s):  
Paul M. Gordon ◽  
Dongmei Liu ◽  
Maureen A. Sartor ◽  
Heidi B. IglayReger ◽  
Emidio E. Pistilli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Resistance Exercise ◽  
Immune Activation ◽  
Biceps Brachii ◽  
Training Session ◽  
Protective Role ◽  
Acute Bout ◽  
Expression Of Genes ◽  
Molecular Events

The primary aim of this investigation was to evaluate the effect of training on the immune activation in skeletal muscle in response to an acute bout of resistance exercise (RE). Seven young healthy men and women underwent a 12-wk supervised progressive unilateral arm RE training program. One week after the last training session, subjects performed an acute bout of bilateral RE in which the trained and the untrained arm exercised at the same relative intensity. Muscle biopsies were obtained 4 h postexercise from the biceps brachii of both arms and assessed for global transcriptom using Affymetrix U133 plus 2.0 microarrays. Significantly regulated biological processes and gene groups were analyzed using a logistic regression-based method following differential (trained vs. untrained) gene expression testing via an intensity-based Bayesian moderated t-test. The results from the present study suggest that training blunts the transcriptional upregulation of immune activation by minimizing expression of genes involved in monocyte recruitment and enhancing gene expression involved in macrophage anti-inflammatory polarization. Additionally, our data suggest that training blunts the transcriptional upregulation of the stress response and the downregulation of glucose metabolism, mitochondrial structure, and oxidative phosphorylation, and it enhances the transcriptional upregulation of the extracellular matrix and cytoskeleton development and organization and the downregulation of gene transcription and muscle contraction. This study provides novel insight into the molecular processes involved in the adaptive response of skeletal muscle following RE training and the cellular and molecular events implicating the protective role of training on muscle stress and damage inflicted by acute mechanical loading.

scholarly journals Hypoxia reprograms calcium signaling and regulates myoglobin expression

2009 ◽  
Vol 296 (3) ◽  
pp. C393-C402 ◽  
Author(s):  
Shane B. Kanatous ◽  
Pradeep P. A. Mammen ◽  
Paul B. Rosenberg ◽  
Cindy M. Martin ◽  
Michael D. White ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Calcium Signaling ◽  
Calcium Influx ◽  
Fiber Type ◽  
Oxygen Storage ◽  
In Vivo Studies ◽  
Calcium Stores ◽  
Activated T Cells

Myoglobin is an oxygen storage molecule that is selectively expressed in cardiac and slow-twitch skeletal muscles that have a high oxygen demand. Numerous studies have implicated hypoxia in the regulation of myoglobin expression as an adaptive response to hypoxic stress. However, the details of this relationship remain undefined. In the present study, adult mice exposed to 10% oxygen for periods up to 3 wk exhibited increased myoglobin expression only in the working heart, whereas myoglobin was either diminished or unchanged in skeletal muscle groups. In vitro and in vivo studies revealed that hypoxia in the presence or absence of exercise-induced stimuli reprograms calcium signaling and modulates myoglobin gene expression. Hypoxia alone significantly altered calcium influx in response to cell depolarization or depletion of endoplasmic reticulum calcium stores, which inhibited the expression of myoglobin. In contrast, our whole animal and transcriptional studies indicate that hypoxia in combination with exercise enhanced the release of calcium from the sarcoplasmic reticulum via the ryanodine receptors triggered by caffeine, which increased the translocation of nuclear factor of activated T-cells into the nucleus to transcriptionally activate myoglobin expression. The present study unveils a previously unrecognized mechanism where the hypoxia-mediated regulation of calcium transients from different intracellular pools modulates myoglobin gene expression. In addition, we observed that changes in myoglobin expression, in response to hypoxia, are not dependent on hypoxia-inducible factor-1 or changes in skeletal muscle fiber type. These studies enhance our understanding of hypoxia-mediated gene regulation and will have broad applications for the treatment of myopathic diseases.

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