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Aberrant iNOS signaling is under genetic control in rodent liver cancer and potentially prognostic for the human disease.

https://arctichealth.org/en/permalink/ahliterature92898
Source
Carcinogenesis. 2008 Aug;29(8):1639-47
Publication Type
Article
Date
Aug-2008
Author
Calvisi Diego F
Pinna Federico
Ladu Sara
Pellegrino Rossella
Muroni Maria R
Simile Maria M
Frau Maddalena
Tomasi Maria L
De Miglio Maria R
Seddaiu Maria A
Daino Lucia
Sanna Valeria
Feo Francesco
Pascale Rosa M
Author Affiliation
Department of Biomedical Sciences, Division of Experimental Pathology and Oncology, University of Sassari, 07100 Sassari, Italy.
Source
Carcinogenesis. 2008 Aug;29(8):1639-47
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Animals
Carcinoma, Hepatocellular - enzymology - epidemiology - genetics - pathology
Cell Line, Tumor
Genetic Predisposition to Disease
Humans
Incidence
Liver Neoplasms - enzymology - epidemiology - genetics - pathology
Male
Mice
Mice, Transgenic
Nitric Oxide Synthase Type II - genetics
Prognosis
Rats
Rats, Inbred BN
Rats, Inbred F344
Signal Transduction - physiology
Abstract
Mounting evidence underlines the role of inducible nitric oxide synthase (iNOS) in hepatocellular carcinoma (HCC) development, but its functional interactions with pathways involved in HCC progression remain uninvestigated. Here, we analyzed in preneoplastic and neoplastic livers from Fisher 344 and Brown Norway rats, possessing different genetic predisposition to HCC, in transforming growth factor-alpha (TGF-alpha) and c-Myc-TGF-alpha transgenic mice, characterized by different susceptibility to HCC, and in human HCC: (i) iNOS function and interactions with nuclear factor-kB (NF-kB) and Ha-RAS/extracellular signal-regulated kinase (ERK) during hepatocarcinogenesis; (ii) influence of genetic predisposition to liver cancer on these pathways and role of these cascades in determining a susceptible or resistant phenotype and (iii) iNOS prognostic value in human HCC. We found progressive iNos induction in rat and mouse liver lesions, always at higher levels in the most aggressive models represented by HCC of rats genetically susceptible to hepatocarcinogenesis and c-Myc-TGF-alpha transgenic mice. iNOS, inhibitor of kB kinase/NF-kB and RAS/ERK upregulation was significantly higher in HCC with poorer prognosis (as defined by patients' survival length) and positively correlated with tumor proliferation, genomic instability and microvascularization and negatively with apoptosis. Suppression of iNOS signaling by aminoguanidine led to decreased HCC growth and NF-kB and RAS/ERK expression and increased apoptosis both in vivo and in vitro. Conversely, block of NF-kB signaling by sulfasalazine or short interfering RNA (siRNA) or ERK signaling by UO126 caused iNOS downregulation in HCC cell lines. These findings indicate that iNOS cross talk with NF-kB and Ha-RAS/ERK cascades influences HCC growth and prognosis, suggesting that key component of iNOS signaling could represent important therapeutic targets for human HCC.
PubMed ID
18579559 View in PubMed
Less detail

Age-related deficit in load-induced skeletal muscle growth.

https://arctichealth.org/en/permalink/ahliterature89394
Source
J Gerontol A Biol Sci Med Sci. 2009 Jun;64(6):618-28
Publication Type
Article
Date
Jun-2009
Author
Hwee Darren T
Bodine Sue C
Author Affiliation
Department of Neurobiology, Physiology, and Behavior, University of California, Davis, 95616, USA.
Source
J Gerontol A Biol Sci Med Sci. 2009 Jun;64(6):618-28
Date
Jun-2009
Language
English
Publication Type
Article
Keywords
Adaptation, Physiological
Age Factors
Aging - physiology
Animals
Caloric Restriction
Hindlimb - physiology
Hindlimb Suspension - physiology
Male
Models, Animal
Muscle Development - physiology
Muscle Proteins - metabolism
Muscle, Skeletal - growth & development
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Inbred F344
Signal Transduction - physiology
Weight-Bearing - physiology
Abstract
The growth response of ankle flexor and extensor muscles to two models of increased loading, functional overload (FO) and hind-limb reloading following hind-limb suspension, was measured by wet weight in Fisher 344-Brown Norway rats at ages ranging from 6 to 30 months. In response to FO, there was a 40% decrease in absolute growth of the plantaris beginning in middle age. Interestingly, the growth response to FO of 30-month old rats maintained on a 40% calorie-restricted diet improved by more than twofold relative to 30-month old rats on a normal chow diet. Recovery of muscle mass upon reloading following disuse was significantly impaired (reduced 7-16%) in predominantly fast, but not slow, muscles of 30-month relative to 9-month old rats. Initial investigation of the Akt signaling pathway following FO suggests a reduction or delay in activation of Akt and its downstream targets in response to increased loading in old rats.
PubMed ID
19351696 View in PubMed
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Aging influences multiple indices of oxidative stress in the heart of the Fischer 344/NNia x Brown Norway/BiNia rat.

https://arctichealth.org/en/permalink/ahliterature83665
Source
Redox Rep. 2007;12(4):167-80
Publication Type
Article
Date
2007
Author
Asano Shinichi
Rice Kevin M
Kakarla Sunil
Katta Anjaiah
Desai Devashish H
Walker Ernest M
Wehner Paulette
Blough Eric R
Author Affiliation
Department of Biological Sciences, Marshall University, Huntington, West Virginia 25755-1090, USA.
Source
Redox Rep. 2007;12(4):167-80
Date
2007
Language
English
Publication Type
Article
Keywords
Aging - physiology
Aldehydes - metabolism
Analysis of Variance
Animals
Blood Pressure - physiology
Female
Heart - physiopathology
Heat-Shock Proteins - metabolism
Immunoblotting
Immunohistochemistry
Male
Microscopy, Fluorescence
Mitogen-Activated Protein Kinases - metabolism
Myocardium - metabolism - pathology
Oxidative Stress
Phosphorylation
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Inbred BN
Rats, Inbred F344
Reactive Oxygen Species - metabolism
Regression Analysis
Signal Transduction - physiology
Superoxides - metabolism
Tyrosine - analogs & derivatives - metabolism
Abstract
We report the influence of aging on multiple markers of oxidative-nitrosative stress in the heart of adult (6-month), aged (30-month) and very aged (36-month) Fischer 344/NNiaHSd x Brown Norway/BiNia (F344/NXBN) rats. Compared to adult (6-month) hearts, indices of oxidative (superoxide anion [O2*-], 4-hydroxy-2-nonenal [4-HNE]) and nitrosative (protein nitrotyrosylation) stress were 34.1 +/- 28.1%, 186 +/- 28.1% and 94 +/- 5.8% higher, respectively, in 36-month hearts and these findings were highly correlated with increases in left ventricular wall thickness (r > 0.669; r > 0.710 and P
PubMed ID
17705987 View in PubMed
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Association of PTPN22 1858T/T genotype with type 1 diabetes, Graves' disease but not with rheumatoid arthritis in Russian population.

https://arctichealth.org/en/permalink/ahliterature135533
Source
Aging (Albany NY). 2011 Apr;3(4):368-73
Publication Type
Article
Date
Apr-2011
Author
Daria Zhebrun
Yulia Kudryashova
Alina Babenko
Alexei Maslyansky
Natalya Kunitskaya
Daria Popcova
Alexandra Klushina
Elena Grineva
Anna Kostareva
Evgeny Shlyakhto
Author Affiliation
Laboratory of Immunology, Almazov Federal Heart, Blood and Endocrinology Center, Saint-Petersburg, Russia.
Source
Aging (Albany NY). 2011 Apr;3(4):368-73
Date
Apr-2011
Language
English
Publication Type
Article
Keywords
Arthritis, Rheumatoid - enzymology - genetics
Case-Control Studies
Diabetes Mellitus, Type 1 - enzymology - genetics
European Continental Ancestry Group - genetics
Gene Frequency
Genetic Predisposition to Disease
Genotype
Graves Disease - enzymology - genetics
Humans
Polymorphism, Single Nucleotide
Protein Tyrosine Phosphatase, Non-Receptor Type 22 - genetics
Russia
Signal Transduction - physiology
Abstract
The protein tyrosine phosphatase nonreceptor 22 gene (PTPN22) is an important negative regulator of signal transduction through the T-cell receptors (TCR). Recently a single-nucleotide polymorphism (SNP) 1858 C/T within this gene was shown to be a risk factor for several autoimmune diseases, such as rheumatoid arthritis (RA), Graves' Disease (GD), systemic lupus erythematosus (SLE), Wegener's granulomatosis (WG) and type 1 diabetes mellitus (T1D). The aim of this study was to analyze a possible association between 1858 C/T SNP and a number of autoimmune diseases, including RA, GD and T1D in Russian population. Patients with T1D, GD, RA and healthy controls were genotyped for the 1858 C/T SNP in PTPN22 gene. We found a significant association between PTPN22 1858 C/T SNP and T1D and GD. 1858T/T genotype was observed more frequently in T1D and GD patients compared to control subjects. No such association was observed for RA. In concordance with a previous data establishing PTPN22 1858 C/T SNP association with several autoimmune diseases, our findings provide further evidence that the PTPN22 gene may play an important role in the susceptibility to some autoimmune diseases.
Notes
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PubMed ID
21467606 View in PubMed
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Bradykinin inhibits development of myocardial infarction through B2 receptor signalling by increment of regional blood flow around the ischaemic lesions in rats.

https://arctichealth.org/en/permalink/ahliterature53623
Source
Br J Pharmacol. 2003 Jan;138(1):225-33
Publication Type
Article
Date
Jan-2003
Author
Hiroshi Ito
Izumi Hayashi
Tohru Izumi
Masataka Majima
Author Affiliation
Department of Pharmacology, Kitasato University School of Medicine, Kitasato 1-15-1, Sagamihara, Kanagawa 228-8555, Japan.
Source
Br J Pharmacol. 2003 Jan;138(1):225-33
Date
Jan-2003
Language
English
Publication Type
Article
Keywords
Animals
Bradykinin - metabolism
Comparative Study
Coronary Circulation - physiology
Kininogens - deficiency - genetics
Male
Myocardial Infarction - metabolism - pathology - prevention & control
Myocardial Ischemia - metabolism - pathology
Rats
Rats, Inbred BN
Rats, Sprague-Dawley
Receptor, Bradykinin B2
Receptors, Bradykinin - antagonists & inhibitors - physiology
Research Support, Non-U.S. Gov't
Signal Transduction - physiology
Abstract
1 To identify the roles of endogenous kinins in prevention of myocardial infarction (MI), we performed the permanent ligation of coronary artery in rats. 2 The size of MI 12, 24, and 48 h after coronary ligation in kininogen-deficient Brown Norway Katholiek (BN-Ka) rats was significantly larger (49.7+/-0.2%, 49.6+/-2%, and 51.1+/-1%, respectively) than that of kinin-replete Brown Norway Kitasato (BN-Ki) rats (42+/-2%, 38.5+/-4%, and 41.5+/-1%). 3 Hoe140, a bradykinin (BK) B(2) receptor antagonist injected (1.0 mg kg(-1), i.v.) half an hour before, and every 8 h after, coronary ligation, significantly increased the size of MI in Sprague-Dawley rats. Aprotinin, a kallikrein inhibitor, which was infused intravenously (10,000 Units kg(-1) h(-1)) with an osmotic mini-pump, significantly increased the size of an MI 24 h after ligation. 4 When evaluated using microspheres, the regional myocardial blood flow around the necrotic lesion in BN-Ka rats 6 h after ligation was reduced more than that in BN-Ki rats with MI by 41-46%. The same was true in Hoe140-treated BN-Ki rats. 5 FR190997, a nonpeptide B(2) agonist, which was infused (10 microg kg(-1) h(-1)) into the vena cava of BN-Ka rats for 24 h with an osmotic mini-pump, caused significant reduction in the size of MI (38+/-3%), in comparison with the size in vehicle solution-treated rats (51+/-3%). The size of MI in FR190997-treated BN-Ka rats was the same as in BN-Ki rats. 6 These results suggested that endogenous kinin has the capacity to reduce the size of MI via B(2) receptor signalling because of the increase in regional myocardial blood flow around the ischaemic lesion.
PubMed ID
12522094 View in PubMed
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Brown Norway rats show impaired nNOS-mediated information transfer in renal autoregulation.

https://arctichealth.org/en/permalink/ahliterature90439
Source
Can J Physiol Pharmacol. 2009 Jan;87(1):29-36
Publication Type
Article
Date
Jan-2009
Author
Wang Xuemei
Cupples William A
Author Affiliation
Lady Davis Institute for Medical Research, SMBD-Jewish General Hospital, Montreal, Quebec, Canada.
Source
Can J Physiol Pharmacol. 2009 Jan;87(1):29-36
Date
Jan-2009
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Animals
Blood Pressure - drug effects
Homeostasis
Male
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - physiology
Nitric Oxide Synthase Type I - physiology
Phenylephrine - pharmacology
Rats
Rats, Inbred BN
Rats, Wistar
Renal Circulation
Signal Transduction - physiology
Abstract
Nonselective inhibition of NO synthase (NOS) augments myogenic autoregulation of renal blood flow (RBF) and profoundly reduces RBF. Previously in Wistar rats, we showed that augmented autoregulation, but not vasoconstriction, is duplicated by intrarenal inhibition of neuronal NOS (nNOS), whereas intrarenal inhibition of inducible NOS (iNOS) has no effect on RBF or on RBF dynamics. Thus macula densa nNOS transfers information from tubuloglomerular feedback to the afferent arteriole. This information flow requires that macula densa nNOS can sufficiently alter ambient NO concentration, that is, that endothelial NOS (eNOS) and iNOS do not alter local NO concentration. Because the Brown Norway rat often shows exaggerated responses to NOS inhibition and has peculiarities of renal autoregulation that are related to NO, we used this strain to study systemic and renal vascular responses to NOS inhibition. The first experiment showed transient blood pressure reduction by bolus i.v. acetylcholine that was dose-dependent in both strains and substantially prolonged in Brown Norway rats. The depressor response decayed more rapidly after nonselective NOS inhibition and the difference between strains was lost, indicating a greater activity of eNOS in Brown Norway rats. In Brown Norway rats, selective inhibition of iNOS reduced RBF (-16% +/- 7%) and augmented myogenic autoregulation, whereas nNOS inhibition reduced RBF (-25% +/- 4%) and did not augment myogenic autoregulation. The significant responses to intrarenal iNOS inhibition, the reduced modulation of autoregulation by nNOS inhibition, and the enhanced endothelial depressor response suggest that physiological signalling by NO within the kidney is impaired in Brown Norway rats because of irrelevant or inappropriate input of NO by eNOS and iNOS.
PubMed ID
19142213 View in PubMed
Less detail

Calcium signal prolongation in sensory neurones of mice with experimental diabetes.

https://arctichealth.org/en/permalink/ahliterature48384
Source
Neuroreport. 1995 May 9;6(7):1010-2
Publication Type
Article
Date
May-9-1995
Author
E. Kostyuk
N. Pronchuk
A. Shmigol
Author Affiliation
Bogomoletz Institute of Physiology, National Academy of Sciences, Kiev, Ukraine.
Source
Neuroreport. 1995 May 9;6(7):1010-2
Date
May-9-1995
Language
English
Publication Type
Article
Keywords
Animals
Calcium - physiology
Calcium Channels - physiology
Diabetes Mellitus, Experimental - pathology - physiopathology
Ganglia, Spinal - cytology - physiopathology
Mice
Mice, Inbred C57BL
Neurons, Afferent - physiology - ultrastructure
Nociceptors - physiology
Signal Transduction - physiology
Abstract
Depolarization-induced Ca2+ transients were studied in dorsal root ganglion neurones of different size (large, 30-45 microns; small, 18-25 microns in diameter) from normal and diabetic mice. Whereas in large neurones no definite changes in the amplitude and time course of the transients were observed, in small neurones the decay of transient became substantially prolonged during streptozotocin-induced and spontaneously occurring diabetes. As small and large neurones differ substantially in their mechanisms of Ca2+ transient termination, we conclude that the prolongation of Ca2+ transients, probably induced by chronic hyperglycaemia, is specific only for small sensory neurones (transmitting mostly nociceptive signals) and may be a cause of the increased pain sensitivity often accompanying this disease.
PubMed ID
7632883 View in PubMed
Less detail

[Changes in calcium signaling in mammalian nociceptive neurons in diabetes mellitus]

https://arctichealth.org/en/permalink/ahliterature47952
Source
Fiziol Zh. 1999;45(4):48-54
Publication Type
Article
Date
1999
Author
N V Voitenko
O P Kostiuk
I A Kruhlykov
N V Svichar
V O Shymkin
Author Affiliation
A. A. Bogomoletz Institute of Physiology, National Academy of Science of the Ukraine, Kiev.
Source
Fiziol Zh. 1999;45(4):48-54
Date
1999
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Calcium - physiology
Comparative Study
Cytosol - physiology
Diabetes Mellitus, Experimental - physiopathology
English Abstract
Fluorescent Dyes
Fura-2
Ganglia, Spinal - physiopathology
Indoles
Mice
Neurons - physiology
Nociceptors - physiopathology
Rats
Research Support, Non-U.S. Gov't
Signal Transduction - physiology
Spinal Cord - physiopathology
Abstract
The changes in neuronal Ca2+ homeostasis were studied on dorsal horn neurons from spinal cord rat slices and freshly isolated dorsal root ganglion neurons of mice in control condition and under streptozotocin (STZ)-induced diabetes. The cytoplasmic free Ca2+ concentration ([Ca2+]i) was measured using fura-2 and indo-1 based microfluorimetry. The recovery of depolarization-induced [Ca2+]i increase was delayed in diabetic neurons compared with normal animals. The amplitude of calcium release from caffeine-sensitive endoplasmic reticulum calcium stores became significantly smaller in diabetic neurons. The participation of mitochondria in [Ca2+]i homeostasis was determined by investigation of changes which occurred after addition of mitochondrial protonophore (CCCP) to the extracellular solution. In control cells 10 (M CCCP applied before membrane depolarization induced an increase of the amplitude of depolarization-induced [Ca2+]i transients and disappearance of their delayed recovery, indicating the participation of mitochondria in fast uptake of Ca2+ ions from the cytosol during the peak of the transient and subsequent slow release them back during its decay. In neurons from diabetic animals the increase of the peak transient amplitude under the action of CCCP became diminished, and the delayed elevation of [Ca2+]i disappeared in small size neurons. We conclude that streptozotocin-induced diabetes is associated with prominent changes in the mechanisms responsible for [Ca2+]i regulation in neurones of the nociceptive system, which presumably include a slow down of Ca2+ elimination from the cytoplasm by endoplasmic reticulum and mitochondria.
PubMed ID
10474802 View in PubMed
Less detail

Changes in calcium signalling in dorsal horn neurons in rats with streptozotocin-induced diabetes.

https://arctichealth.org/en/permalink/ahliterature47921
Source
Neuroscience. 1999;94(3):887-90
Publication Type
Article
Date
1999
Author
N V Voitenko
E P Kostyuk
I A Kruglikov
P G Kostyuk
Author Affiliation
Department of General Physiology of the Nervous System, Bogomoletz Institute of Physiology, Kiev, Ukraine. nana@serv.biph.kiev.ua
Source
Neuroscience. 1999;94(3):887-90
Date
1999
Language
English
Publication Type
Article
Keywords
Animals
Caffeine - pharmacology
Calcium - physiology
Cytoplasm - metabolism
Diabetes Mellitus, Experimental - physiopathology
Fluorescent Dyes
Fura-2 - analogs & derivatives
In Vitro
Male
Membrane Potentials - drug effects
Posterior Horn Cells - drug effects - physiology
Potassium Chloride - pharmacology
Rats
Rats, Wistar
Reference Values
Research Support, Non-U.S. Gov't
Signal Transduction - physiology
Spinal Cord - physiology - physiopathology
Abstract
Intracellular calcium signalling was studied in the dorsal horn from neurons of rats with streptozotocin-induced diabetes versus control animals. The cytoplasmic Ca2+ concentration ([Ca2+]i) was measured in Fura-2 acetoxymethyl ester-loaded dorsal horn neurons from acutely isolated spinal cord slices using a fluorescence technique. The recovery of depolarization-induced [Ca2+]i increase was delayed in diabetic neurons compared with normal animals. In normal neurons, [Ca2+]i after the end of KCl depolarization recovered to the basal level monoexponentially with a time constant of 8.0+/-0.5 s (n = 23), while diabetic neurons showed two exponentials in the [Ca2+]i recovery. The time constants of these exponentials were 7.2+/-0.5 and 23.0+/-0.6 s (n = 19), respectively. The amplitude of calcium release from caffeine-sensitive endoplasmic reticulum calcium stores became significantly smaller in diabetic neurons. The amplitudes of [Ca2+]i transients evoked by 30 mM caffeine were 268+/-29 nM (n = 13) and 31+/-9 nM (n = 17) in control and diabetic neurons, respectively. We conclude that streptozotocin-induced diabetes is associated with prominent changes in the mechanisms responsible for [Ca2+]i regulation, which presumably include a slowdown of Ca2+ elimination from the cytoplasm by the endoplasmic reticulum.
PubMed ID
10579579 View in PubMed
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Contraction-mediated mTOR, p70S6k, and ERK1/2 phosphorylation in aged skeletal muscle.

https://arctichealth.org/en/permalink/ahliterature49689
Source
J Appl Physiol. 2004 Jul;97(1):243-8
Publication Type
Article
Date
Jul-2004
Author
Jascha D Parkington
Nathan K LeBrasseur
Adam P Siebert
Roger A Fielding
Author Affiliation
Department of Health Sciences, Boston University, Boston, MA 02215, USA.
Source
J Appl Physiol. 2004 Jul;97(1):243-8
Date
Jul-2004
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Blotting, Western
Electric Stimulation
Female
Male
Mitogen-Activated Protein Kinase 1 - physiology
Mitogen-Activated Protein Kinase 3 - physiology
Muscle Contraction - physiology
Muscle, Skeletal - enzymology - growth & development - physiology
Organ Size - drug effects - physiology
Phosphorylation
Protein Kinases - physiology
Rats
Rats, Inbred BN
Rats, Inbred F344
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Ribosomal Protein S6 Kinases, 70-kDa - physiology
Sciatic Nerve - physiology
Signal Transduction - physiology
Abstract
With age, skeletal muscle experiences substantial atrophy and weakness. Although resistance training can increase muscle size and strength, the myogenic response to exercise and the capacity for muscle hypertrophy in older humans and animals is limited. In the present study, we assessed the ability of muscle contractile activity to activate cellular pathways involved in muscle cell growth and myogenesis in adult (Y; 6 mo old) and aged (O; 30 mo old) Fischer 344 x Brown Norway rats. A single bout of rat hindlimb muscle contractile activity was elicited by high-frequency electrical stimulation (HFES) of the sciatic nerve. Plantaris (Pla) and tibialis anterior (TA) muscles were assayed for mammalian target of rapamycin (mTOR), 70-kDa ribosomal protein S6 kinase (p70(S6K)), and extracellular signal-regulated kinase (ERK) 1/2 phosphorylation and total protein either at baseline, immediately after, or 6 h after HFES. mTOR phosphorylation was elevated in Pla (1.3 +/- 0.3-fold, P
PubMed ID
15033970 View in PubMed
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31 records – page 1 of 4.