Publications
139 results found
Shore AM, Karamitri A, Kemp P, et al., 2013, Cold-Induced Changes in Gene Expression in Brown Adipose Tissue, White Adipose Tissue and Liver, PLOS One, Vol: 8, ISSN: 1932-6203
Cold exposure imposes a metabolic challenge to mammals that is met by a coordinated response in different tissues to prevent hypothermia. This study reports a transcriptomic analysis in brown adipose tissue (BAT), white adipose (WAT) and liver of mice in response to 24 h cold exposure at 8°C. Expression of 1895 genes were significantly (P<0.05) up- or down-regulated more than two fold by cold exposure in all tissues but only 5 of these genes were shared by all three tissues, and only 19, 14 and 134 genes were common between WAT and BAT, WAT and liver, and BAT and liver, respectively. We confirmed using qRT-PCR, the increased expression of a number of characteristic BAT genes during cold exposure. In both BAT and the liver, the most common direction of change in gene expression was suppression (496 genes in BAT and 590 genes in liver). Gene ontology analysis revealed for the first time significant (P<0.05) down regulation in response to cold, of genes involved in oxidoreductase activity, lipid metabolic processes and protease inhibitor activity, in both BAT and liver, but not WAT. The results reveal an unexpected importance of down regulation of cytochrome P450 gene expression and apolipoprotein, in both BAT and liver, but not WAT, in response to cold exposure. Pathway analysis suggests a model in which down regulation of the nuclear transcription factors HNF4α and PPARα in both BAT and liver may orchestrate the down regulation of genes involved in lipoprotein and steroid metabolism as well as Phase I enzymes belonging to the cytochrome P450 group in response to cold stress in mice. We propose that the response to cold stress involves decreased gene expression in a range of cellular processes in order to maximise pathways involved in heat production.
Natanek SA, Riddoch-Contreras J, Marsh GS, et al., 2013, MuRF-1 and Atrogin-1 Protein Expression and Quadriceps Fiber Size and Muscle Mass in Stable Patients with COPD, Copd-Journal of Chronic Obstructive Pulmonary Disease, Vol: 10, Pages: 618-624, ISSN: 1541-2563
Jackson AS, Shrikrishna D, Kelly JL, et al., 2013, Vitamin D and skeletal muscle strength and endurance in COPD (vol 41, pg 309, 2013), EUROPEAN RESPIRATORY JOURNAL, Vol: 41, Pages: 998-998, ISSN: 0903-1936
Bloch SAA, Lee JY, Wort SJ, et al., 2013, Sustained Elevation of Circulating Growth and Differentiation Factor-15 and a Dynamic Imbalance in Mediators of Muscle Homeostasis Are Associated With the Development of Acute Muscle Wasting Following Cardiac Surgery, CRITICAL CARE MEDICINE, Vol: 41, Pages: 982-989, ISSN: 0090-3493
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- Citations: 59
Jackson AS, Shrikrishna D, Kelly JL, et al., 2013, Vitamin D and skeletal muscle strength and endurance in COPD, EUROPEAN RESPIRATORY JOURNAL, Vol: 41, Pages: 309-316, ISSN: 0903-1936
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- Citations: 37
Hopkinson NS, Shrikrishna D, Tanner RJ, et al., 2013, The Effect Of Angiotensin-Converting Enzyme Inhibition On Skeletal Muscle Dysfunction In Chronic Obstructive Pulmonary Disease: A Randomized Controlled Trial, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 187, ISSN: 1073-449X
Patel MS, Donaldson AV, Lewis A, et al., 2013, Serum And Quadriceps Expression Of Klotho In Smokers And COPD Patients, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 187, ISSN: 1073-449X
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- Citations: 1
Shrikrishna D, Tanner RJ, Lee JY, et al., 2012, THE EFFECT OF ANGIOTENSIN-CONVERTING ENZYME INHIBITION ON SKELETAL MUSCLE DYSFUNCTION IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE: A RANDOMISED CONTROLLED TRIAL, Winter Meeting of the British-Thoracic-Society 2012, Publisher: BMJ PUBLISHING GROUP, Pages: A25-A25, ISSN: 0040-6376
Bloch SAA, Lee JY, Wort SJ, et al., 2012, CIRCULATING REGULATORS OF ACUTE MUSCLE WASTING IN THE CRITICALLY ILL: GDF-15 A POTENTIAL NOVEL DRIVER OF ACUTE MUSCLE WASTING, Winter Meeting of the British-Thoracic-Society 2012, Publisher: BMJ PUBLISHING GROUP, Pages: A37-A37, ISSN: 0040-6376
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- Citations: 2
Maddocks M, Shrikrishna D, Vitoriano S, et al., 2012, PHYSICAL INACTIVITY IS ASSOCIATED WITH MID-THIGH INTRAMUSCULAR FAT IN PATIENTS WITH COPD, Winter Meeting of the British-Thoracic-Society 2012, Publisher: BMJ PUBLISHING GROUP, Pages: A98-A98, ISSN: 0040-6376
Shrikrishna D, Patel M, Tanner RJ, et al., 2012, Quadriceps wasting and physical inactivity in patients with COPD, EUROPEAN RESPIRATORY JOURNAL, Vol: 40, Pages: 1115-1122, ISSN: 0903-1936
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- Citations: 235
Shrikrishna D, Astin R, Kemp PR, et al., 2012, Renin-angiotensin system blockade: a novel therapeutic approach in chronic obstructive pulmonary disease, CLINICAL SCIENCE, Vol: 123, Pages: 487-498, ISSN: 0143-5221
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- Citations: 61
Bloch S, Polkey MI, Griffiths M, et al., 2012, Molecular mechanisms of intensive care unit-acquired weakness, EUROPEAN RESPIRATORY JOURNAL, Vol: 39, Pages: 1000-1011, ISSN: 0903-1936
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- Citations: 50
Riddoch-Contreras J, George T, Natanek SA, et al., 2012, p38 Mitogen-activated Protein Kinase is Not Activated in the Quadriceps of Patients with Stable Chronic Obstructive Pulmonary Disease, COPD-JOURNAL OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE, Vol: 9, Pages: 142-150, ISSN: 1541-2555
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- Citations: 15
Hyde MJ, Mostyn A, Modi N, et al., 2012, The health implications of birth by Caesarean section, BIOLOGICAL REVIEWS, Vol: 87, Pages: 229-243, ISSN: 1464-7931
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- Citations: 141
Lewis A, Riddoch-Contreras J, Natanek SA, et al., 2012, Downregulation of the serum response factor/miR-1 axis in the quadriceps of patients with COPD, THORAX, Vol: 67, Pages: 26-34, ISSN: 0040-6376
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- Citations: 118
Natanek SA, 2012, PATHWAYS ASSOCIATED WITH REDUCED QUADRICEPSOXIDATIVE FIBRES AND ENDURANCE IN COPD, European Respiratory Journal
Rationale: Reduced quadriceps endurance in COPD is associated with apredominance of type II glycolytic over type I oxidative fibres (fibre shift, FS) andreduced muscle energy stores. Molecular mechanisms responsible for thisremain unknown. We hypothesised that expression of known regulators of type Ifibres and energy production in quadriceps muscle would differ in COPD patientswith and without FS.Methods: We measured lung function, physical activity, exercise performance,quadriceps strength and endurance (non-volitionally) in 38 GOLD Stage I-IVCOPD patients and 23 healthy age-matched controls. Participants had aquadriceps biopsy; type I and II fibre proportions were determined usingimmunohistochemistry and FS defined using published reference ranges.Calcineurin A, phosphorylated adenosine monophosphate kinase-alpha(phospho-AMPK) and protein kinase A-alpha catalytic subunits were measuredby western blotting and modulators of calcineurin activity, calmodulin, 14-3-3proteins, and myocyte-enriched calcineurin-interacting protein-1 mRNAmeasured by western blotting and qPCR respectively. Downstream, nuclearmyocyte enhancer factor-2 capable of DNA-binding was quantified bytranscription factor ELISA.European Respiratory Journal Page 2 of 96123456789101112131415161718192021222324252627282930313233343536373839404142434445464748495051525354555657585960Page 3 of 31Results: Unexpectedly calcineurin expression was higher, while phospho-AMPKwas lower, in COPD patients with than without FS. Phospho-AMPK levelscorrelated with quadriceps endurance in patients.Conclusions: Reduced phospho-AMPK may contribute to reduced quadricepsoxidative capacity and endurance in COPD.
Lee JY, Hopkinson NS, Kemp PR, 2011, Myostatin induces autophagy in skeletal muscle <i>in vitro</i>, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 415, Pages: 632-636, ISSN: 0006-291X
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- Citations: 43
Donaldson AVJ, Lewis A, Natanek A, et al., 2011, INCREASED SKELETAL MUSCLE-SPECIFIC MICRORNA-1 IN THE BLOOD OF COPD PATIENTS, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A25-A25, ISSN: 0040-6376
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- Citations: 3
Amanda Natanek S, Riddoch-Contreras J, Sarah Marsh G, et al., 2011, Yin Yang 1 expression and localisation in quadriceps muscle in COPD, ARCHIVOS DE BRONCONEUMOLOGIA, Vol: 47, Pages: 296-302, ISSN: 0300-2896
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- Citations: 21
Harling L, Warren OJ, Martin A, et al., 2011, Do Miniaturized Extracorporeal Circuits Confer Significant Clinical Benefit Without Compromising Safety? A Meta-Analysis of Randomized Controlled Trials, ASAIO JOURNAL, Vol: 57, Pages: 141-151, ISSN: 1058-2916
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- Citations: 36
Hyde MJ, Clarke L, Griffin JL, et al., 2011, A single enteral feed prior to the commencement of parenteral nutrition ameliorates the incidence of steatosis in parenterally fed neonatal piglets, METABOLOMICS, Vol: 7, Pages: 118-125, ISSN: 1573-3882
Thickitt A, Fainberg P, Clarke L, et al., 2011, Impact of route of delivery upon regulators of adipose tissue lipid metabolism in the pig, PROCEEDINGS OF THE NUTRITION SOCIETY, Vol: 70, Pages: E28-E28, ISSN: 0029-6651
Natanek SA, Langen RCJ, Gosker HR, et al., 2010, NF-KAPPA B (NF-κB) AND ACTIVATOR PROTEIN-1 (AP-1) DNA BINDING IN THE QUADRICEPS OF COPD PATIENTS, Publisher: B M J PUBLISHING GROUP, Pages: A138-A139, ISSN: 0040-6376
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- Citations: 1
Natanek SA, Gosker HR, Slot I, et al., 2010, MUSCLE FIBRE ATROPHY AND AEROBIC TO ANAEROBIC FIBRE TYPE SHIFT IN THE QUADRICEPS IN COPD, Publisher: B M J PUBLISHING GROUP, Pages: A139-A139, ISSN: 0040-6376
Man W-C, Natanek SA, Riddoch-Contreras J, et al., 2010, Quadriceps myostatin expression in COPD, European Respiratory Journal, Vol: 36, Pages: 686-688
Shore A, Karamitri A, Kemp P, et al., 2010, Role of Ucp1 enhancer methylation and chromatin remodelling in the control of Ucp1 expression in murine adipose tissue, Diabetologia, Vol: 53, Pages: 1164-1173, ISSN: 0012-186X
Aims/hypothesisIncreasing the expression of the brown adipose tissue-specific gene uncoupling protein-1 (Ucp1) is a potential target for treating obesity. We investigated the role of DNA methylation and histone modification in Ucp1 expression in adipose cell lines and ex vivo murine adipose tissues.MethodsMethylation state of the Ucp1 enhancer was studied using bisulphite mapping in murine adipose cell lines, and tissue taken from cold-stressed mice, coupled with functional assays of the effects of methylation and demethylation of the Ucp1 promoter on gene expression and nuclear protein binding.ResultsWe show that demethylation of the Ucp1 promoter by 5-aza-deoxycytidine increases Ucp1 expression while methylation of Ucp1 promoter–reporter constructs decreases expression. Brown adipose tissue-specific Ucp1 expression is associated with decreased CpG dinucleotide methylation of the Ucp1 enhancer. The lowest CpG dinucleotide methylation state was found in two cyclic AMP response elements (CRE3, CRE2) in the Ucp1 promoter and methylation of the CpG in CRE2, but not CRE3 decreased nuclear protein binding. Chromatin immunoprecipitation assays revealed the presence of the silencing DiMethH3K9 modification on the Ucp1 enhancer in white adipose tissue and the appearance of the active TriMethH3K4 mark at the Ucp1 promoter in brown adipose tissue in response to a cold environment.Conclusions/interpretationThe results demonstrate that CpG dinucleotide methylation of the Ucp1 enhancer exhibits tissue-specific patterns in murine tissue and cell lines and suggest that adipose tissue-specific Ucp1 expression involves demethylation of CpG dinucleotides found in regulatory CREs in the Ucp1 enhancer, as well as modification of histone tails.
Amirak E, Zakkar M, Evans PC, et al., 2010, Perfusion of veins at arterial pressure increases the expression of KLF5 and cell cycle genes in smooth muscle cells, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol: 391, Pages: 818-823, ISSN: 0006-291X
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- Citations: 4
Amirak E, Zakkar M, Evans PC, et al., 2010, Perfusion of veins at arterial pressure increases the expression of KLF5 and cell cycle genes in smooth muscle cells., Biochem Biophys Res Commun, Vol: 391, Pages: 818-823
Vascular smooth muscle cell (VSMC) proliferation remains a major cause of veno-arterial graft failure. We hypothesised that exposure of venous SMCs to arterial pressure would increase KLF5 expression and that of cell cycle genes. Porcine jugular veins were perfused at arterial or venous pressure in the absence of growth factors. The KLF5, c-myc, cyclin-D and cyclin-E expression were elevated within 24h of perfusion at arterial pressure but not at venous pressure. Arterial pressure also reduced the decline in SM-myosin heavy chain expression. These data suggest a role for KLF5 in initiating venous SMCs proliferation in response to arterial pressure.
Lewis A, Riddoch-Contreras J, Natanek SA, et al., 2010, Alterations in MRTF and FHL1 activity contribute to fibre type shift in the quadriceps of patients with COPD., Publisher: AMER THORACIC SOC, ISSN: 1073-449X
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- Citations: 1
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