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Abnormal regulation of the LDL-R and HMG CoA reductase genes in subjects with familial hypercholesterolemia with the "French Canadian mutation".

https://arctichealth.org/en/permalink/ahliterature211598
Source
Atherosclerosis. 1996 Jul;124(1):103-17
Publication Type
Article
Date
Jul-1996
Author
L. Yu
S. Qiu
J. Genest
Author Affiliation
Cardiovascular Genetics Laboratory, Clinical Research Institute of Montréal, Québec Canada.
Source
Atherosclerosis. 1996 Jul;124(1):103-17
Date
Jul-1996
Language
English
Publication Type
Article
Keywords
Anticholesteremic Agents - pharmacology - therapeutic use
Canada - epidemiology
Cells, Cultured
Enzyme Induction
Enzyme Inhibitors - pharmacology - therapeutic use
Ethnic Groups - genetics
Female
Fibroblasts - metabolism
France - ethnology
Gene Expression Regulation - drug effects
Haploidy
Humans
Hydroxymethylglutaryl CoA Reductases - genetics
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Hyperlipoproteinemia Type II - drug therapy - ethnology - genetics
Lipoproteins, LDL - metabolism
Lovastatin - pharmacology - therapeutic use
Male
Prevalence
RNA, Messenger - biosynthesis - genetics
Receptors, LDL - genetics - metabolism
Sequence Deletion
Transcription, Genetic
Treatment Failure
Abstract
Familial hypercholesterolemia (FH) is seen with high frequency in the province of Québec, Canada. A large deletion (> 10 kb) of the 5'-end of the low density lipoprotein receptor (LDL-R) gene is the major mutation of the LDL-R in FH subjects in Québec (approximately 60% of FH subjects). No mRNA is produced from the allele bearing the mutation, and cellular cholesterol obtained by receptor-mediated endocytosis is under the control of the non-deletion allele. We have previously reported that some patients with the 10-kb deletion (approximately 9%) fail to respond to the hydroxymethylglutaryl coenzyme A reductase (HMG CoA reductase) inhibitor class of medications. We studied mRNA levels of the LDL-R and HMG CoA reductase genes in response to the HMG CoA reductase inhibitor lovastatin in a time- and dose-dependent fashion in cultured human skin fibroblasts and we devised an in vitro model to study the response to drug therapy in subjects with FH. We determined mRNA levels by RNase protection assay in skin fibroblasts obtained from controls (n = 3) and FH subjects with the > 10-kb deletion (responders, n = 3; non responders, n = 3; to drug therapy). We measured 125I-LDL binding on skin fibroblasts grown in the presence of lipoprotein-deficient serum with or without 1 microM lovastatin, using 10 micrograms/mL of 125I-LDL protein. Control subjects exhibited coordinate regulation of the LDL-R and HMG CoA reductase genes in response to lovastatin, 0.1-25 microM, for 0-24 h. Correlation coefficients between mRNA levels of both genes were > 0.9 in controls and FH subjects. However, by linear regression analysis, the corresponding slopes for the correlation between both genes were 0.98 (controls), 3.36 and 3.63 (FH responders and non-responders), indicating a pattern of dissociated but still coordinate regulation in FH subjects. The magnitude of increase of mRNA levels of the LDL-R gene was approximately five-fold over LPDS in controls, two-fold in FH responders and two-fold in non-responders. Binding studies using 125I-LDL reveal that a control subject and all responders had a 2-2.5-fold increase in binding to cell surface receptors but two out of three FH non-responders showed no increase in binding in response to 1 microM lovastatin. The LDL-R and HMG CoA reductase genes are expressed in coordinate regulation in fibroblasts from subjects with FH due to the > 10-kb deletion, but with a proportionately greater up-regulation of the HMG CoA reductase gene. Some subjects, with FH caused by the > 10-kb deletion of the LDL-R gene, who fail to respond to HMG CoA reductase inhibitors have abnormal LDL receptor binding activity at the cell surface in response to lovastatin in vitro.
PubMed ID
8800498 View in PubMed
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Aging and susceptibility to toluene in rats: a pharmacokinetic, biomarker, and physiological approach.

https://arctichealth.org/en/permalink/ahliterature98359
Source
J Toxicol Environ Health A. 2010;73(4):301-18
Publication Type
Article
Date
2010
Author
Christopher J Gordon
Reddy R Gottipolu
Elaina M Kenyon
Ronald Thomas
Mette C Schladweiler
Cina M Mack
Jonathan H Shannahan
J Grace Wallenborn
Abraham Nyska
Robert C MacPhail
Judy E Richards
Mike Devito
Urmila P Kodavanti
Author Affiliation
National Health and Environmental Effects Research Laboratory, ORD, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, USA. Gordon.christopher@epa.gov
Source
J Toxicol Environ Health A. 2010;73(4):301-18
Date
2010
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Biological Markers
Brain - metabolism
Dose-Response Relationship, Drug
Gene Expression Regulation - drug effects
Glutathione Peroxidase - genetics - metabolism
Glutathione Transferase - genetics - metabolism
Heart - drug effects
Male
Myocardium - metabolism
Rats
Superoxide Dismutase - genetics - metabolism
Toluene - blood - pharmacokinetics - toxicity
Abstract
Aging adults are a growing segment of the U.S. population and are likely to exhibit increased susceptibility to many environmental toxicants. However, there is little information on the susceptibility of the aged to toxicants. The toxicity of toluene has been well characterized in young adult rodents but there is little information in the aged. Three approaches were used: (1) pharmacokinetic (PK), (2) cardiac biomarkers, and (3) whole-animal physiology to assess whether aging increases susceptibility to toluene in the Brown Norway (BN) rat. Three life stages, young adult, middle aged, and aged (4, 12, and 24 mo, respectively), were administered toluene orally at doses of 0, 0.3, 0.65, or 1 g/kg and subjected to the following: terminated at 45 min or 4 h post dosing, and blood and brain toluene concentration were measured; terminated at 4 h post dosing, and biomarkers of cardiac function were measured; or monitor heart rate (HR), core temperature (Tc), and motor activity (MA) by radiotelemetry before and after dosing. Brain toluene concentration was significantly elevated in aged rats at 4 h after dosing with either 0.3 or 1 g/kg. Blood toluene concentrations were unaffected by age. There were various interactions between aging and toluene-induced effects on cardiac biomarkers. Most notably, toluene exposure led to reductions in mRNA markers for oxidative stress in aged but not younger animals. Toluene also produced a reduction in cardiac endothelin-1 in aged rats. Higher doses of toluene led to tachycardia, hypothermia, and a transient elevation in MA. Aged rats were less sensitive to the tachycardic effects of toluene but showed a prolonged hypothermic response. Elevated brain levels of toluene in aged rats may be attributed to their suppressed cardiovascular and respiratory responses. The expression of several cardiac biochemical markers of toluene exposure in the aged may also reflect differential susceptibility to this toxicant.
PubMed ID
20077299 View in PubMed
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Anti-inflammatory effects of tectroside on UVB-induced HaCaT cells.

https://arctichealth.org/en/permalink/ahliterature114711
Source
Int J Mol Med. 2013 Jun;31(6):1471-6
Publication Type
Article
Date
Jun-2013
Author
Sung-Bae Kim
Ok-Hwa Kang
Dae-Ki Joung
Su-Hyun Mun
Yun-Soo Seo
Mi-Ran Cha
Shi-Yong Ryu
Dong-Won Shin
Dong-Yeul Kwon
Author Affiliation
Institute of Biotechnology, Wonkwang University, Jeonbuk, Republic of Korea.
Source
Int J Mol Med. 2013 Jun;31(6):1471-6
Date
Jun-2013
Language
English
Publication Type
Article
Keywords
Anti-Inflammatory Agents - chemistry - pharmacology
Asteraceae - chemistry
Cell Line
Cell Survival - drug effects - radiation effects
Cyclooxygenase 2 - genetics
Gene Expression Regulation - drug effects
Humans
Interleukin-6 - biosynthesis
Interleukin-8 - biosynthesis
Keratinocytes - drug effects - metabolism - radiation effects
Lactones - chemistry - pharmacology
Mitogen-Activated Protein Kinases - metabolism
Phosphorylation
Plant Extracts - chemistry - pharmacology
RNA, Messenger - genetics
Sesquiterpenes, Guaiane - chemistry - pharmacology
Ultraviolet Rays - adverse effects
Abstract
Ultraviolet B (UVB) irradiation causes skin damage and inflammation by inducing the secretion of various cytokines, which are immune regulators produced by cells. To prevent skin inflammation, keratinocytes that have been irreversibly damaged by UVB must be eliminated through apoptosis. Ixeris dentata (I.?dentata) (family Asteraceae) is a perennial medicinal herb indigenous to Korea. It is used in Korea, China and Japan to treat indigestion, pneumonia, diabetes, hepatitis, contusions and tumors. Guaiane-type sesquiterpene lactones were isolated from the whole extract of I.?dentata. This led to the isolation of the anti-inflammatory sesquiterpene lactone compound tectroside (TES), which was tested on a human keratinocyte cell line. To determine the anti-inflammatory effects of TES, we examined its influence on UVB-induced pro-inflammatory cytokine production in human keratinocytes (HaCaT cells) by observing these cells in the presence or absence of TES. In the present study, pro-inflammatory cytokine production was determined by performing enzyme-linked immunosorbent assay, reverse transcription-polymerase chain reaction and western blot analysis to evaluate the activation of mitogen-activated protein kinases (MAPKs). TES inhibited UVB-induced production of the pro-inflammatory cytokines interleukin (IL)-6 and IL-8 in a dose-dependent manner. In addition, TES inhibited the expression of cyclooxygenase (COX)-2 and the phosphorylation of c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) MAPKs, suggesting that it inhibits the secretion of the pro-inflammatory cytokines IL-6 and IL-8 and COX-2 expression by blocking MAPK phosphorylation. These results suggest that TES can potentially protect against UVB-induced skin inflammation.
PubMed ID
23588209 View in PubMed
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Association between IL-1beta/TNF-alpha-induced glucocorticoid-sensitive changes in multiple gene expression and altered responsiveness in airway smooth muscle.

https://arctichealth.org/en/permalink/ahliterature10091
Source
Am J Respir Cell Mol Biol. 2001 Dec;25(6):761-71
Publication Type
Article
Date
Dec-2001
Author
H. Hakonarson
E. Halapi
R. Whelan
J. Gulcher
K. Stefansson
M M Grunstein
Author Affiliation
DeCode Genetics, Reykjavik, Iceland. hakonh@decode.is
Source
Am J Respir Cell Mol Biol. 2001 Dec;25(6):761-71
Date
Dec-2001
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Animals
Asthma - physiopathology
Comparative Study
Dexamethasone - pharmacology
Gene Expression Profiling
Gene Expression Regulation - drug effects
Interleukin-1 - pharmacology
Isoproterenol - pharmacology
Muscle Contraction - drug effects
Muscle Relaxation - drug effects
Muscle, Smooth - cytology - drug effects - metabolism
Oligonucleotide Array Sequence Analysis
RNA, Messenger - biosynthesis
Rabbits
Research Support, U.S. Gov't, P.H.S.
Signal Transduction - drug effects - physiology
Trachea - cytology - drug effects - metabolism
Transcription Factors - genetics - metabolism
Tumor Necrosis Factor-alpha - pharmacology
Abstract
The pleiotropic cytokines interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha have been implicated in the pathophysiology of asthma. To elucidate the role of these cytokines in the pro-asthmatic state, the effects of IL-1beta and TNF-alpha on airway smooth muscle (ASM) responsiveness and ASM expression of multiple genes, assessed by high-density oligonucleotide array analysis, were examined in the absence and presence of the glucocorticoid dexamethasone (DEX). Administration of IL-1beta/TNF-alpha increased ASM contractility to acetylcholine and impaired ASM relaxation to isoproterenol. These pro-asthmatic- like changes in ASM responsiveness were associated with IL-1beta/ TNF-alpha-induced mRNA expression of a host of proinflammatory genes that regulate transcription, cytokines and chemokines, cellular adhesion molecules, and various signal transduction molecules that regulate ASM responsiveness. In the presence of DEX, the changes induced in ASM responsiveness were abrogated, and most of the IL-1beta/TNF-alpha-mediated changes in proinflammatory gene expression were repressed, although mRNA expression of a small number of genes was enhanced by DEX. Collectively, the observations support the concept that, together with its role as a regulator of airway tone, in response to IL-1beta/TNF-alpha, the ASM expresses a host of glucocorticoid-sensitive genes that contribute to the altered structure and function of the airways in the pro-asthmatic state. We speculate that glucocorticoid-sensitive, cytokine-induced pathways involved in ASM cell signaling represent important targets for new therapeutic interventions.
PubMed ID
11726403 View in PubMed
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Associations between gastrointestinal toxicity, micro RNA and cytokine production in patients undergoing myeloablative allogeneic stem cell transplantation.

https://arctichealth.org/en/permalink/ahliterature268773
Source
Int Immunopharmacol. 2015 Mar;25(1):180-8
Publication Type
Article
Date
Mar-2015
Author
Peter L Pontoppidan
Karina Jordan
Anting Liu Carlsen
Hilde Hylland Uhlving
Katrine Kielsen
Mette Christensen
Marianne Ifversen
Claus Henrik Nielsen
Per Sangild
Niels Henrik Helweg Heegaard
Carsten Heilmann
Henrik Sengeløv
Klaus Müller
Source
Int Immunopharmacol. 2015 Mar;25(1):180-8
Date
Mar-2015
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Biomarkers - metabolism
Cells, Cultured
Child
Child, Preschool
Citrulline - blood
Cytokines - blood
Denmark
Drug Therapy
Enterocytes - drug effects - immunology
Gene Expression Regulation - drug effects
Hematopoietic Stem Cell Transplantation
Humans
Infant
Inflammation Mediators - blood
Intestines - pathology
Leukocytes, Mononuclear - drug effects - immunology
Lymphocyte Activation - drug effects
Male
MicroRNAs - genetics - immunology - metabolism
Middle Aged
Myeloablative Agonists - therapeutic use
Prospective Studies
Transplantation Conditioning - methods
Young Adult
Abstract
Allogeneic hematopoietic stem cell transplantation (HSCT) is a procedure with a high risk of treatment related mortality. The primary aim of the present study was to examine associations between markers of gastrointestinal toxicity, markers of systemic inflammation, and plasma levels of microRNA (miRNA) -155 and -146a during the first month after HSCT. The secondary aim was to characterize the impact of the toxic-inflammatory response on the function of circulating leukocytes during immune recovery. Thirty HSCT patients were included. Gastrointestinal injury was monitored by toxicity scores, lactulose-mannitol test and plasma citrulline, as a measure of the enterocyte population. Nadir of citrulline and maximum of oral toxicity scores, intestinal permeability, CRP and plasma levels of IL-6 and IL-10 was seen at day +7 post-HSCT. miRNA-155 and mi-RNA-146a showed an inverse relation with significantly elevated miRNA-155 and decreased miRNA-146a levels, from day 0 to day +28 compared with pre-conditioning levels. Citrulline levels below the median at day +7 were associated with higher spontaneous production of IL-6 and TNF-a as well as higher in vitro stimulated production of IL-17A at day +21. This study is the first to demonstrate that toxic responses to chemotherapy are accompanied by differential regulation of miRNAs with opposing effects on immune regulation. We find that a proinflammatory miRNA profile is sustained during the first three weeks after the transplantation, indicating that these miRNAs may play a role in the regulation of the inflammatory environment during immune reconstitution after HSCT.
PubMed ID
25614225 View in PubMed
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Beneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how?

https://arctichealth.org/en/permalink/ahliterature3153
Source
Prostaglandins Leukot Essent Fatty Acids. 2000 Dec;63(6):351-62
Publication Type
Article
Date
Dec-2000
Author
U N Das
Author Affiliation
EFA Sciences LLC, 1420 Providence Highway, Norwood, MA 02062, USA. undurti@hotmail.com
Source
Prostaglandins Leukot Essent Fatty Acids. 2000 Dec;63(6):351-62
Date
Dec-2000
Language
English
Publication Type
Article
Keywords
Acetylcholine - physiology
Animals
Arrhythmia - epidemiology - prevention & control
Brain - physiopathology
Cardiovascular Diseases - diet therapy - epidemiology - prevention & control
Cell Adhesion Molecules - biosynthesis - genetics
Cell Division - drug effects
Clinical Trials
Cohort Studies
Cytokines - metabolism
Dietary Fats - administration & dosage - pharmacology - therapeutic use
Eicosanoids - metabolism
Endothelium, Vascular - drug effects - metabolism
Exercise
Fatty Acids, Omega-3 - administration & dosage - pharmacology - therapeutic use
Fatty Acids, Unsaturated - metabolism
Fish Oils - administration & dosage - pharmacology - therapeutic use
Gene Expression Regulation - drug effects
Greenland - epidemiology
Heart - drug effects
Hemostasis - drug effects
Humans
Hypothalamo-Hypophyseal System - drug effects - physiopathology
Inflammation - drug therapy - metabolism - prevention & control
Inuits
Japan - epidemiology
Lipid Metabolism
Models, Biological
Myocardium - metabolism
Oxidation-Reduction
Oxidative Stress
Parasympathetic Nervous System - drug effects
Pituitary-Adrenal System - drug effects - physiopathology
Rats
Sodium Channels - drug effects
Vagus Nerve - physiopathology
Abstract
Low rates of coronary heart disease was found in Greenland Eskimos and Japanese who are exposed to a diet rich in fish oil. Suggested mechanisms for this cardio-protective effect focused on the effects of n-3 fatty acids on eicosanoid metabolism, inflammation, beta oxidation, endothelial dysfunction, cytokine growth factors, and gene expression of adhesion molecules; But, none of these mechanisms could adequately explain the beneficial actions of n-3 fatty acids. One attractive suggestion is a direct cardiac effect of n-3 fatty acids on arrhythmogenesis. N-3 fatty acids can modify Na+ channels by directly binding to the channel proteins and thus, prevent ischemia-induced ventricular fibrillation and sudden cardiac death. Though this is an attractive explanation, there could be other actions as well. N-3 fatty acids can inhibit the synthesis and release of pro-inflammatory cytokines such as tumor necrosis factoralpha (TNFalpha) and interleukin-1 (IL-1) and IL-2 that are released during the early course of ischemic heart disease. These cytokines decrease myocardial contractility and induce myocardial damage, enhance the production of free radicals, which can also suppress myocardial function. Further, n-3 fatty acids can increase parasympathetic tone leading to an increase in heart rate variability and thus, protect the myocardium against ventricular arrhythmias. Increased parasympathetic tone and acetylcholine, the principle vagal neurotransmitter, significantly attenuate the release of TNF, IL-1beta, IL-6 and IL-18. Exercise enhances parasympathetic tone, and the production of anti-inflammatory cytokine IL-10 which may explain the beneficial action of exercise in the prevention of cardiovascular diseases and diabetes mellitus. TNFalpha has neurotoxic actions, where as n-3 fatty acids are potent neuroprotectors and brain is rich in these fatty acids. Based on this, it is suggested that the principle mechanism of cardioprotective and neuroprotective action(s) of n-3 fatty acids can be due to the suppression of TNFalpha and IL synthesis and release, modulation of hypothalamic-pituitary-adrenal anti-inflammatory responses, and an increase in acetylcholine release, the vagal neurotransmitter. Thus, there appears to be a close interaction between the central nervous system, endocrine organs, cytokines, exercise, and dietary n-3 fatty acids. This may explain why these fatty acids could be of benefit in the management of conditions such as septicemia and septic shock, Alzheimer's disease, Parkinson's disease, inflammatory bowel diseases, diabetes mellitus, essential hypertension and atherosclerosis.
Notes
Erratum In: Prostaglandins Leukot Essent Fatty Acids 2001 Jan;64(1):74
PubMed ID
11133172 View in PubMed
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Black currant seed oil supplementation of mothers enhances IFN-? and suppresses IL-4 production in breast milk.

https://arctichealth.org/en/permalink/ahliterature107756
Source
Pediatr Allergy Immunol. 2013 Sep;24(6):562-6
Publication Type
Article
Date
Sep-2013
Author
Pia Linnamaa
Kaisa Nieminen
Leena Koulu
Saska Tuomasjukka
Heikki Kallio
Baoru Yang
Raija Tahvonen
Johannes Savolainen
Author Affiliation
Department of Dermatology, University of Turku, Turku, Finland.
Source
Pediatr Allergy Immunol. 2013 Sep;24(6):562-6
Date
Sep-2013
Language
English
Publication Type
Article
Keywords
Breast Feeding
Dermatitis, Atopic - immunology - therapy
Diet Therapy
Dietary Supplements
Female
Finland
Follow-Up Studies
Gene Expression Regulation - drug effects - immunology
Humans
Infant
Infant, Newborn
Interferon-gamma - genetics - immunology - metabolism
Interleukin-4 - genetics - immunology - metabolism
Milk, Human - immunology - metabolism
Mothers
Plant Oils - administration & dosage
Pregnancy
Ribes
Seeds
Th1-Th2 Balance - drug effects
Abstract
The first year of infancy is crucial for the development of atopic immune response. Inadequate early Th1 and Treg responses and increased production of Th2 cytokines are associated with atopy. Breast milk contains several immunomodulatory cytokines and other factors that might influence the maturation of the infant's immune system. We assessed the cytokines in breast milk of mother of newborn infants and their associations with black currant seed oil (BCSO) supplementation during pregnancy, mother's atopic status and the development of infant's atopic dermatitis.
Mothers and infants from an intervention study by black currant seed oil (n = 31) or olive oil as placebo (n = 30) were included in the study. Breast milk samples were collected during the first 3 months of breastfeeding. Breast milk levels of IL-4, IL-5, IL-10, IL-12, IFN-? and TNF were measured by Luminex technology.
BCSO intervention group had decreased level of IL-4 (p = 0.044) and elevated level of IFN-? (p = 0.014) in breast milk as compared to olive oil group. No significant differences were observed in IL-5, IL-10, IL-12 and TNF levels between the BCSO and olive oil groups. Mothers who had atopic dermatitis had significantly decreased levels of IL-10 (p = 0.044) in breast milk. Breast milk of the mothers of the children who developed atopic dermatitis had lower levels of IFN-? (p = 0.039) as compared to the breast milk of the mothers of the children without dermatitis.
Dietary intervention with BCSO had immunomodulatory effects on breast milk cytokine production towards Th2 to Th1 immunodeviation.
PubMed ID
23980846 View in PubMed
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Calcium-calmodulin kinase II is the common factor in calcium-dependent cardiac expression and secretion of A- and B-type natriuretic peptides.

https://arctichealth.org/en/permalink/ahliterature78613
Source
Endocrinology. 2007 Jun;148(6):2815-20
Publication Type
Article
Date
Jun-2007
Author
Ronkainen Jarkko J
Vuolteenaho Olli
Tavi Pasi
Author Affiliation
University of Oulu, Department of Physiology and Biocenter Oulu, University of Oulu, 90014 Oulu, Finland.
Source
Endocrinology. 2007 Jun;148(6):2815-20
Date
Jun-2007
Language
English
Publication Type
Article
Keywords
Animals
Animals, Newborn
Atrial Natriuretic Factor - genetics - metabolism - secretion
Benzylamines - pharmacology
Ca(2+)-Calmodulin Dependent Protein Kinase - genetics - metabolism - physiology
Calcium - pharmacology
Cells, Cultured
Gene Expression Regulation - drug effects
Male
Myocytes, Cardiac - drug effects - metabolism
Natriuretic Peptide, Brain - genetics - metabolism - secretion
Rats
Rats, Sprague-Dawley
Sulfonamides - pharmacology
Abstract
Peptides derived from the precursor of A- and B-type natriuretic peptides (ANP and BNP) are powerful clinical markers of cardiac hypertrophy and dysfunction. It is known that many stimuli affecting the intracellular calcium concentration also induce ANP and BNP secretion. It was our intention to study the mechanisms by which calcium regulates the secretion of ANP and BNP. The effects of pacing and calcium-calmodulin kinase II activity on natriuretic peptide secretion were studied in isolated perfused rat atria and cultured rat neonatal cardiomyocytes. In isolated rat atrium pacing induced an increase in diastolic, systolic, and averaged intracellular free calcium concentration and a frequency-dependent increase in the secretion of both ANP and BNP. The molar ratio of the secreted natriuretic peptides (ANP to BNP) remained nearly constant ( approximately 1000) at all the pacing frequencies tested (1, 3, 6, and 8 Hz). Calmodulin kinase II inhibitor KN-93 (3 mum) did not affect intracellular free calcium concentration but showed a frequency-dependent inhibitory effect on ANP and BNP secretion without a change in ANP to BNP ratio. In the neonatal cardiomyocytes, KN-93 (3 mum) suppressed the secretion and gene expression of both ANP and BNP. Overexpression of constitutively active (T286D) or nuclear (delta(B)) calcium-calmodulin kinase II induced an increase in ANP and BNP gene expression. The results indicate that the calcium-dependent secretion and gene expression of A- and B-type natriuretic peptides are similarly regulated by calmodulin kinase II-dependent mechanisms. This is a plausible mechanism contributing to exercise-induced natriuretic peptide secretion and the augmented secretion in heart dysfunction due to impaired calcium handling.
PubMed ID
17332063 View in PubMed
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Control of beta 3-adrenergic receptor gene expression in brown adipocytes in culture.

https://arctichealth.org/en/permalink/ahliterature11423
Source
Mol Cell Endocrinol. 1995 Apr 1;109(2):189-95
Publication Type
Article
Date
Apr-1-1995
Author
S. Klaus
P. Muzzin
J P Revelli
M A Cawthorne
J P Giacobino
D. Ricquier
Author Affiliation
Fachbereich Biologie/Zoologie, Philipps Universität, Marburg, Germany.
Source
Mol Cell Endocrinol. 1995 Apr 1;109(2):189-95
Date
Apr-1-1995
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Agonists - pharmacology
Animals
Base Sequence
Brown Fat - cytology - drug effects - metabolism
Cell Differentiation
Cells, Cultured
Cricetinae
Ethanolamines - pharmacology
Gene Expression Regulation - drug effects
Half-Life
Isoproterenol - pharmacology
Molecular Sequence Data
Phodopus
Receptors, Adrenergic, beta - biosynthesis - genetics
Receptors, Adrenergic, beta-3
Research Support, Non-U.S. Gov't
Abstract
Brown adipose tissue is a mammalian thermogenic tissue. Its ability to dissipate energy as heat is due to a unique mitochondrial protein, uncoupling protein (UCP). Activation and expression of UCP is under control of the sympathetic nervous system acting through beta -adrenergic receptors (AR). In this study we used Siberian hamster brown adipocytes differentiated in vitro to investigate the expression of the fat specific beta 3-AR. Binding studies using the new labelled beta 3 adrenergic ligand [3H]SB 206606 showed a density of beta 3-AR in brown adipocyte plasma membranes comparable to that measured in vivo. beta 3-AR mRNA expression was very high in mature brown adipocytes and was started to be expressed during differentiation before UCP mRNA. Its half-life was approximately 50 min. Treatment of cells with non-specific beta adrenergic agonists, specific beta 3-adrenergic agonists, and dibutyryl cyclic AMP resulted in a marked down regulation of beta 3-AR mRNA level within several hours.
PubMed ID
7664982 View in PubMed
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Dietary fish protein alters blood lipid concentrations and hepatic genes involved in cholesterol homeostasis in the rat model.

https://arctichealth.org/en/permalink/ahliterature80453
Source
Br J Nutr. 2006 Oct;96(4):674-82
Publication Type
Article
Date
Oct-2006
Author
Shukla Anjali
Bettzieche Anja
Hirche Frank
Brandsch Corinna
Stangl Gabriele I
Eder Klaus
Author Affiliation
Institute of Nutritional Sciences, Martin-Luther-University of Halle-Wittenberg, Emil-Abderhalden-Strasse 26, D-06108 Halle/Saale, Germany.
Source
Br J Nutr. 2006 Oct;96(4):674-82
Date
Oct-2006
Language
English
Publication Type
Article
Keywords
Amino Acids - analysis - blood
Animals
Cholesterol - blood
Diet
Dietary Proteins - pharmacology
Fatty Acids - analysis
Fish Proteins - pharmacology
Food Analysis - methods
Gene Expression Regulation - drug effects
Homeostasis - genetics
Lipid Metabolism - drug effects - genetics
Lipids - blood
Liver - metabolism
Male
RNA, Messenger - genetics
Rats
Rats, Sprague-Dawley
Triglycerides - blood
Abstract
It is known that various dietary plant proteins are capable of influencing the lipid metabolism of human subjects and animals when compared with casein. Less, however, is known about the effects of fish protein on the cholesterol and triacylglycerol metabolism. Therefore, two experiments were conducted in which rats were fed diets containing 200 g of either fish protein, prepared from Alaska pollack fillets, or casein, which served as control, per kilogram, over 20 and 22 d, respectively. As parameters of lipid metabolism, the concentrations of cholesterol and triacylglycerols in the plasma and liver, the faecal excretion of bile acids and the hepatic expression of genes encoding proteins involved in lipid homeostasis were determined. In both experiments, rats fed fish protein had higher concentrations of cholesteryl esters in the liver, a lower concentration of cholesterol in the HDL fraction (rho > 1.063 kg/l) and lower plasma triacylglycerol concentrations than rats fed casein (P
PubMed ID
17010226 View in PubMed
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36 records – page 1 of 4.