16 results match your criteria argii activity

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Arginase II protein regulates Parkin-dependent p32 degradation that contributes to Ca2+-dependent eNOS activation in endothelial cells.

Cardiovasc Res 2021 May 8. Epub 2021 May 8.

Department of Biological Sciences.

Aims: Arginase II (ArgII) plays a key role in the regulation of Ca2+ between the cytosol and mitochondria in a p32-dependent manner. p32 contributes to endothelial nitric oxide synthase (eNOS) activation through the Ca2+/CaMKII/AMPK/p38MAPK/Akt signaling cascade. Therefore, we investigated a novel function of ArgII in the regulation of p32 stability. Read More

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Arginase II activity regulates cytosolic Ca level in a p32-dependent manner that contributes to Ca-dependent vasoconstriction in native low-density lipoprotein-stimulated vascular smooth muscle cells.

Exp Mol Med 2019 06 3;51(6):1-12. Epub 2019 Jun 3.

Department of Biology, School of Medicine, Kangwon National University, Chuncheon, 24341, South Korea.

Although arginase II (ArgII) is abundant in mitochondria, Ca-accumulating organelles, the relationship between ArgII activity and Ca translocation into mitochondria and the regulation of cytosolic Ca signaling are completely unknown. We investigated the effects of ArgII activity on mitochondrial Ca uptake through mitochondrial p32 protein (p32m) and on CaMKII-dependent vascular smooth muscle cell (VSMC) contraction. Native low-density lipoprotein stimulation induced an increase in [Ca]m as measured by CoCl-quenched calcein-AM fluorescence, which was prevented by Arg inhibition in hAoSMCs and reduced in mAoSMCs from ArgII mice. Read More

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L-Norvaline Reverses Cognitive Decline and Synaptic Loss in a Murine Model of Alzheimer's Disease.

Neurotherapeutics 2018 10;15(4):1036-1054

Drug Discovery Laboratory, The Azrieli Faculty of Medicine, Bar-Ilan University, 1311502, Safed, Israel.

The urea cycle is strongly implicated in the pathogenesis of Alzheimer's disease (AD). Arginase-I (ARGI) accumulation at sites of amyloid-beta (Aβ) deposition is associated with L-arginine deprivation and neurodegeneration. An interaction between the arginase II (ARGII) and mTOR-ribosomal protein S6 kinase β-1 (S6K1) pathways promotes inflammation and oxidative stress. Read More

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October 2018

Protective Role of Arginase II in Cerebral Ischemia and Excitotoxicity.

J Neurol Neurosci 2016;7(2). Epub 2016 Apr 29.

Department of Anesthesiology, University of Florida, Gainesville, 32610, FL, USA; Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, 32610, FL, USA; Departments of Neurology, Psychiatry, Psychology, Pharmaceutics, and Neuroscience, University of Florida, Gainesville, 32610 FL, USA.

Background: Arginase (Arg), one of the enzymes involved in the urea cycle, provides an essential route for the disposal of excess nitrogen resulting from amino acid and nucleotide metabolism. Two reported subtypes of Arg (ArgI and II) compete with nitric oxide synthase (NOS) to use L-arginine as a substrate, and subsequently regulate NOS activity. It has been reported that Arg has significant effects on circulation that suggest the potential role of this enzyme in regulating vascular function. Read More

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Biphasic Effect of Diabetes on Neuronal Nitric Oxide Release in Rat Mesenteric Arteries.

PLoS One 2016 7;11(6):e0156793. Epub 2016 Jun 7.

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain.

Introduction: We analysed possible time-dependent changes in nitrergic perivascular innervation function from diabetic rats and mechanisms implicated.

Materials And Methods: In endothelium-denuded mesenteric arteries from control and four- (4W) and eight-week (8W) streptozotocin-induced diabetic rats the vasoconstriction to EFS (electrical field stimulation) was analysed before and after preincubation with L-NAME. Neuronal NO release was analysed in the absence and presence of L-arginine, tetrahydrobiopterine (BH4) and L-arginine plus BH4. Read More

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Differential responses of macrophages from bovines naturally resistant or susceptible to Mycobacterium bovis after classical and alternative activation.

Vet Immunol Immunopathol 2013 Jul 6;154(1-2):8-16. Epub 2013 May 6.

Universidad Autónoma de Nuevo León, Departamento de Microbiología e Inmunología, Laboratorio de Inmunología y Virología, Facultad de Ciencias Biológicas, Av. Pedro de Alba S/N, Cd. Universitaria, C.P. 66451 San Nicolás de los Garza, Nuevo León, Mexico.

It is known that macrophages from naturally resistant animals possess a strong immune response against bovine tuberculosis to control mycobacterial infections. In the present study, the macrophage phagocytic activity, intracellular bacterial survival, and cytokine gene expression induced by classical and alternative activators against Mycobacterium bovis in naturally resistant or susceptible bovines, were evaluated. Animals were classified as naturally resistant or susceptible based on the capacity of their macrophages to allow M. Read More

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Nrf2 in bone marrow-derived cells positively contributes to the advanced stage of atherosclerotic plaque formation.

Free Radic Biol Med 2012 Dec 7;53(12):2256-62. Epub 2012 Oct 7.

Department of Stress Response Science, Hirosaki University Graduate School of Medicine, 5 Zaifu-cho, Hirosaki, Aomori 036-8562, Japan. Electronic address:

Atherosclerosis is the major etiology underlying myocardial infarction and stroke, and strategies for preventing atherosclerosis are urgently needed. In the context of atherosclerosis, the deletion of the Nrf2 gene, which encodes a master regulator of the oxidative stress response in mammals, reportedly attenuates atherosclerosis formation. However, the precise mechanisms of protection against atherosclerosis are largely unknown. Read More

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December 2012

Increased arginase II activity contributes to endothelial dysfunction through endothelial nitric oxide synthase uncoupling in aged mice.

Exp Mol Med 2012 Oct;44(10):594-602

Department of Biology College of Natural Sciences Kangwon National University Chuncheon 200-701, Korea.

The incidence of cardiovascular disease is predicted to increase as the population ages. There is accumulating evidence that arginase upregulation is associated with impaired endothelial function. Here, we demonstrate that arginase II (ArgII) is upregulated in aortic vessels of aged mice and contributes to decreased nitric oxide (NO) generation and increased reactive oxygen species (ROS) production via endothelial nitric oxide synthase (eNOS) uncoupling. Read More

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October 2012

Arginase II inhibition prevents nitrate tolerance.

Br J Pharmacol 2012 Aug;166(7):2015-23

Baker IDI Heart and Diabetes Institute, Melbourne, Australia.

Background And Purpose: Nitrate tolerance, the loss of vascular responsiveness with continued use of nitrates, remains incompletely understood and is a limitation of these therapeutic agents. Vascular superoxide, generated by uncoupled endothelial NOS (eNOS), may play a role. As arginase competes with eNOS for L-arginine and may exacerbate the production of reactive oxygen species (ROS), we hypothesized that arginase inhibition might reduce nitrate tolerance. Read More

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Stable overexpression of arginase I and ornithine transcarbamylase in HepG2 cells improves its ammonia detoxification.

J Cell Biochem 2012 Feb;113(2):518-27

Fujian Institute of Hepatobiliary Surgery, Union Hospital, Fujian Medical University, Fuzhou, PR China.

HepG2 is an immortalized human hepatoma cell line that has been used for research into bioartificial liver systems. However, a low level of ammonia detoxification is its biggest drawback. In this work, a recombinant HepG2 cell line with stable overexpression of human arginase I (hArgI) and human ornithine transcarbamylase (hOTC), HepG2/(hArgI + hOTC)4, was developed using a eukaryotic dual gene expression vector pBudCE4. Read More

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February 2012

Model for the exceptional reactivity of peroxiredoxins 2 and 3 with hydrogen peroxide: a kinetic and computational study.

J Biol Chem 2011 May 8;286(20):18048-55. Epub 2011 Mar 8.

Department of Pathology and National Research Centre for Growth and Development, University of Otago Christchurch, P.O. Box 4345, Christchurch, New Zealand.

Peroxiredoxins (Prx) are thiol peroxidases that exhibit exceptionally high reactivity toward peroxides, but the chemical basis for this is not well understood. We present strong experimental evidence that two highly conserved arginine residues play a vital role in this activity of human Prx2 and Prx3. Point mutation of either ArgI or ArgII (in Prx3 Arg-123 and Arg-146, which are ∼3-4 Å or ∼6-7 Å away from the active site peroxidative cysteine (C(p)), respectively) in each case resulted in a 5 orders of magnitude loss in reactivity. Read More

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Structural motifs of importance for the constitutive activity of the orphan 7TM receptor EBI2: analysis of receptor activation in the absence of an agonist.

Mol Pharmacol 2008 Oct 15;74(4):1008-21. Epub 2008 Jul 15.

Laboratory for Molecular Pharmacology, Department of Neuroscience and Pharmacology, The Panum Institute, Copenhagen University, Blegdamsvej 2, 2200 Copenhagen, Denmark.

The Epstein-Barr induced receptor 2 (EBI2) is a lymphocyte-expressed orphan seven transmembrane-spanning (7TM) receptor that signals constitutively through Galphai, as shown, for instance by guanosine 5'-O-(3-thio)triphosphate incorporation. Two regions of importance for the constitutive activity were identified by a systematic mutational analysis of 29 residues in EBI2. The cAMP response element-binding protein transcription factor was used as a measure of receptor activity and was correlated to the receptor surface expression. Read More

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October 2008

Arginase I induction by modified lipoproteins in macrophages: a peroxisome proliferator-activated receptor-gamma/delta-mediated effect that links lipid metabolism and immunity.

Mol Endocrinol 2008 Jun 6;22(6):1394-402. Epub 2008 Mar 6.

Departamento de Bioquímica y Biología Molecular y Genética, Universidad de Extremadura. Avenida de la Universidad s/n, 10071 Cáceres, Spain.

Macrophages are phagocytic cells that play essential roles in innate immunity and lipid homeostasis. The uptake of modified lipoproteins is an important early event in the development of atherosclerosis. We analyzed the ability of modified low-density lipoprotein (LDL) (oxidized and acetylated) to alter the expression and activity of arginases (ArgI and ArgII) in macrophages. Read More

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Mitochondrial arginase II constrains endothelial NOS-3 activity.

Am J Physiol Heart Circ Physiol 2007 Dec 7;293(6):H3317-24. Epub 2007 Sep 7.

Department of Anesthesiology, Johns Hopkins Hospital, The Johns Hopkins Medical Institutions, 600 N. Wolfe St., Baltimore, MD 21287, USA.

Emerging evidence supports the idea that arginase, expressed in the vascular endothelial cells of humans and other species, modulates endothelial nitric oxide (NO) synthase-3 (NOS-3) activity by regulating intracellular L-arginine bioavailability. Arginase II is thought to be expressed in the mitochondria of a variety of nonendothelial cells, whereas arginase I is known to be confined to the cytosol of hepatic and other cells. The isoforms that regulate NOS-3 and their subcellular distribution, however, remain incompletely characterized. Read More

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December 2007

The arginase II gene is an anti-inflammatory target of liver X receptor in macrophages.

J Biol Chem 2006 Oct 30;281(43):32197-206. Epub 2006 Aug 30.

Howard Hughes Medical Institute, Molecular Biology Institute and Department of Pathology and Laboratory Medicine, University of California-Los Angeles, Los Angeles, CA 90095, USA.

The liver X receptors (LXRs) are ligand-dependent transcription factors that have been implicated in lipid metabolism and inflammation. LXRs also inhibit the expression of inflammatory genes in macrophages, including inducible nitric oxide synthase (iNOS). Some of these actions are mediated through LXR antagonism of NF-kappaB activity. Read More

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October 2006

Regulation of arginase II by interferon regulatory factor 3 and the involvement of polyamines in the antiviral response.

FEBS J 2005 Jun;272(12):3120-31

Terry Fox Molecular Oncology Group, Lady Davis Institute for Medical Research, Montreal, Canada.

The innate antiviral response requires the induction of genes and proteins with activities that limit virus replication. Among these, the well-characterized interferon beta (IFNB) gene is regulated through the cooperation of AP-1, NF-kappaB and interferon regulatory factor 3 (IRF-3) transcription factors. Using a constitutively active form of IRF-3, IRF-3 5D, we showed previously that IRF-3 also regulates an IFN-independent antiviral response through the direct induction of IFN-stimulated genes. Read More

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