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ischemia and amino acid

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https://www.readbyqxmd.com/read/28529483/identification-of-a-novel-allosteric-inhibitory-site-on-tryptophan-hydroxylase-1-enabling-unprecedented-selectivity-over-all-related-hydroxylases
#1
Mike Petrassi, Rob Barber, Celine Be, Sarah Beach, Brian Cox, Anne-Marie D'Souza, Nick Duggan, Martin Hussey, Roy Fox, Peter Hunt, Gabor Jarai, Takatoshi Kosaka, Paul Oakley, Viral Patel, Neil Press, David Rowlands, Clemens Scheufler, Oliver Schmidt, Honnappa Srinivas, Mary Turner, Rob Turner, John Westwick, Alison Wolfreys, Nuzhat Pathan, Simon Watson, Matthew Thomas
Pulmonary arterial hypertension (PAH) has demonstrated multi-serotonin receptor dependent pathologies, characterized by increased tone (5-HT1B receptor) and complex lesions (SERT, 5-HT1B, 5-HT2B receptors) of the pulmonary vasculature together with right ventricular hypertrophy, ischemia and fibrosis (5-HT2B receptor). Selective inhibitors of individual signaling elements - SERT, 5-HT2A, 5HT2B, and combined 5-HT2A/B receptors, have all been tested clinically and failed. Thus, inhibition of tryptophan hydroxylase 1 (TPH1), the rate limiting step in 5-HT synthesis, has been suggested as a more broad, and thereby more effective, mode of 5-HT inhibition...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/28524210/sulfur-dioxide-foe-or-friend-for-life
#2
REVIEW
Xin-Bao Wang, Hong Cui, Xiaohong Liu, Jun-Bao Du
Sulfur dioxide (SO₂) is a toxic gas and air pollutant. The toxic effects of SO₂ have been extensively studied. Oxidative damage due to SO2 can occur in multiple organs. Inhaled SO₂ can also cause chromosomal aberrations, DNA damage and gene mutations in mammals. However, SO₂ can also be generated from the sulfur-containing amino acid, L-cysteine. Recent studies have shown that SO₂ has a vasorelaxant effect, and ameliorates pulmonary hypertension and vascular remodeling. SO₂ can also reduce lung injury and myocardial injury in rats...
May 19, 2017: Histology and Histopathology
https://www.readbyqxmd.com/read/28504843/a-novel-synthetic-chemical-entity-upei-800-is-neuroprotective-in-vitro-and-in-an-in-vivo-rat-model-of-oxidative-stress
#3
Tarek M Saleh, Monique C Saleh, Barry J Connell, Inan Kucukkaya, Alaa S Abd-El-Aziz
In this study, we tested a novel synthetic pyrazole-containing compound, 5-amino-1-phenyl-1H-pyrazole-4-carbonitrile (APPC), as an antioxidant in both in vitro and in vivo models of oxidative stress. In addition, the utility of covalently combining APPC with another well-established antioxidant, lipoic acid (LA), was also tested in both models. The in vitro results demonstrated that pretreatment with APPC in a mixed neuronal-glial culture exposed to oxygen-glucose deprivation (OGD) followed by reoxygenation-refeeding, resulted in significant neuroprotection at concentrations between 2...
May 15, 2017: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/28503134/aquaporin-4-mediated-glutamate-induced-astrocyte-swelling-is-partially-mediated-through-metabotropic-glutamate-receptor-5-activation
#4
Zhongfang Shi, Wei Zhang, Yang Lu, Yi Lu, Lixin Xu, Qing Fang, Min Wu, Mei Jia, Yujiao Wang, Liping Dong, Xu Yan, Shaohua Yang, Fang Yuan
Astrocytes are one of the most abundant cell types in the mammalian central nervous system (CNS), and astrocyte swelling is the primary event associated with brain edema. Glutamate, the principal excitatory amino acid neurotransmitter in the CNS, is released at high levels after brain injury including cerebral ischemia. This leads to astrocyte swelling, which we previously demonstrated is related to metabotropic glutamate receptor (mGluR) activation. Aquaporin 4 (AQP4), the predominant water channel in the brain, is expressed in astrocyte endfeet and plays an important role in brain edema following ischemia...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28499867/glycine-nitronyl-nitroxide-conjugate-protects-human-umbilical-vein-endothelial-cells-against-hypoxia-reoxygenation-injury-via-multiple-mechanisms-and-ameliorates-hind-limb-ischemia-reperfusion-injury-in-rats
#5
Xiang Gao, Yue Bi, Kui Chi, Yang Liu, Tao Yuan, Xueyan Li, Wei Bi
Oxidative stress and inflammation play important roles in the pathogenesis of ischemia/reperfusion (I/R)-injury. The administration of antioxidants and anti-inflammatory agents has been applied to prevent I/R-injury for several decades. Of the numerous compounds administrated therapeutically in anti-oxidative stress, nitronyl nitroxide has gained increasing attention due to its continuous ability to scavenge active oxygen radicals. However, its effect is not ideal in clinical therapy. In previous study, we linked the anti-inflammatory amino acid glycine to nitronyl nitroxide and developed a novel glycine-nitronyl nitroxide (GNN) conjugate, which showed a synergetic protection against renal ischemia/reperfusion injury...
June 17, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28487390/activation-of-the-amino-acid-response-pathway-blunts-the-effects-of-cardiac-stress
#6
Pu Qin, Pelin Arabacilar, Roberta E Bernard, Weike Bao, Alan R Olzinski, Yuanjun Guo, Hind Lal, Stephen H Eisennagel, Michael C Platchek, Wensheng Xie, Julius Del Rosario, Mohamad Nayal, Quinn Lu, Theresa Roethke, Christine G Schnackenberg, Fe Wright, Michael P Quaile, Wendy S Halsey, Ashley M Hughes, Ganesh M Sathe, George P Livi, Robert B Kirkpatrick, Xiaoyan A Qu, Deepak K Rajpal, Maria Faelth Savitski, Marcus Bantscheff, Gerard Joberty, Giovanna Bergamini, Thomas L Force, Gregory J Gatto, Erding Hu, Robert N Willette
BACKGROUND: The amino acid response (AAR) is an evolutionarily conserved protective mechanism activated by amino acid deficiency through a key kinase, general control nonderepressible 2. In addition to mobilizing amino acids, the AAR broadly affects gene and protein expression in a variety of pathways and elicits antifibrotic, autophagic, and anti-inflammatory activities. However, little is known regarding its role in cardiac stress. Our aim was to investigate the effects of halofuginone, a prolyl-tRNA synthetase inhibitor, on the AAR pathway in cardiac fibroblasts, cardiomyocytes, and in mouse models of cardiac stress and failure...
May 9, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28486919/metabolic-imbalance-of-homocysteine-and-hydrogen-sulfide-in-kidney-disease
#7
O Karmin, Yaw L Siow
Homocysteine (Hcy) and hydrogen sulfide (H2S) are important molecules produced during the metabolism of sulfur-containing amino acids. Hcy metabolism is central to the supply of methyl groups that are essential for biological function. Hcy can be either regenerated to methionine or metabolized to cysteine, a precursor for glutathione synthesis. Cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) play a crucial role in metabolizing Hcy to cysteine through the transsulfuration pathway. These two enzymes are also responsible for H2S generation through desulfuration reactions...
May 9, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28475986/cdse-zns-zns-quantum-dots-loaded-in-polymeric-micelles-as-a-ph-triggerable-targeting-fluorescence-imaging-probe-for-detecting-cerebral-ischemic-area
#8
Hong Yu Yang, Yan Fu, Moon-Sun Jang, Yi Li, Wen Ping Yin, Tae Kyu Ahn, Jung Hee Lee, Heeyeop Chae, Doo Sung Lee
High photoluminescence (PL) quantum yield (QY), photostability CdSe@ZnS/ZnS core/multishell quantum dots (CM-QDs) were first applied for bioimaging. The solubility, stability and biocompatible of the fluorescence imaging probes were constructed by self-assembly of CM-QDs and pH-responsive methoxy poly(ethylene glycol)-poly(β-amino ester/amidoamine)-dodecylamine (mPEG-PAEA-DDA) multiblock copolymers. The resulting CM-QDs-loaded mPEG-PAEA-DDA micelles (CM-QDs-PEG-PAEA-DDA) exhibited lower cell cytotoxicity and higher fluorescence intensity than the core/shell CdSe@ZnS QDs-encapsulated mPEG-PAEA-DDA micelles (CS-QDs-PEG-PAEA-DDA)...
April 27, 2017: Colloids and Surfaces. B, Biointerfaces
https://www.readbyqxmd.com/read/28456939/genetic-mutation-of-glun2b-protects-brain-cells-against-stroke-damages
#9
Na Tang, Jianhua Wu, Houze Zhu, Honglin Yan, Yu Guo, You Cai, Huanhuan Yan, Yan Shi, Shu Shu, Lei Pei, Youming Lu
Immediately following ischemia, glutamate accumulates in the extracellular space and results in extensive stimulation of its receptors including N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors. A large amount of Ca(2+) influx directly through the receptor-gated ion channels which leads to Ca(2+) overload and triggers several downstream lethal reactions. As a result, cell dies via apoptosis or necrosis, or both. Death-associated protein kinase 1 (DAPK1) physically and functionally interacts with the NMDA receptor GluN2B subunit at extra-synaptic sites and this interaction acts as a central mediator for stroke damage...
April 29, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28442737/structural-and-biochemical-insights-of-cypa-and-aif-interaction
#10
Biancamaria Farina, Gianluigi Di Sorbo, Angela Chambery, Andrea Caporale, Guido Leoni, Rosita Russo, Fabiola Mascanzoni, Domenico Raimondo, Roberto Fattorusso, Menotti Ruvo, Nunzianna Doti
The Cyclophilin A (CypA)/Apoptosis Inducing Factor (AIF) complex is implicated in the DNA degradation in response to various cellular stress conditions, such as oxidative stress, cerebral hypoxia-ischemia and traumatic brain injury. The pro-apoptotic form of AIF (AIF(Δ1-121)) mainly interacts with CypA through the amino acid region 370-394. The AIF(370-394) synthetic peptide inhibits complex formation in vitro by binding to CypA and exerts neuroprotection in a model of glutamate-mediated oxidative stress. Here, the binding site of AIF(Δ1-121) and AIF(370-394) on CypA has been mapped by NMR spectroscopy and biochemical studies, and a molecular model of the complex has been proposed...
April 25, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28423529/pif-promotes-brain-re-myelination-locally-while-regulating-systemic-inflammation-clinically-relevant-multiple-sclerosis-m-smegmatis-model
#11
Giuseppe Migliara, Martin Mueller, Alessia Piermattei, Chaya Brodie, Michael J Paidas, Eytan R Barnea, Francesco Ria
Neurologic disease diagnosis and treatment is challenging. Multiple Sclerosis (MS) is a demyelinating autoimmune disease with few clinical forms and uncertain etiology. Current studies suggest that it is likely caused by infection(s) triggering a systemic immune response resulting in antigen/non-antigen-related autoimmune response in central nervous system (CNS). New therapeutic approaches are needed. Secreted by viable embryos, PreImplantation Factor (PIF) possesses a local and systemic immunity regulatory role...
March 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28414037/spatio-temporal-regulation-of-connexin43-phosphorylation-and-gap-junction-dynamics
#12
REVIEW
Joell L Solan, Paul D Lampe
Gap junctions are specialized membrane domains containing tens to thousands of intercellular channels. These channels permit exchange of small molecules (<1000Da) including ions, amino acids, nucleotides, metabolites and secondary messengers (e.g., calcium, glucose, cAMP, cGMP, IP3) between cells. The common reductionist view of these structures is that they are composed entirely of integral membrane proteins encoded by the 21 member connexin human gene family. However, it is clear that the normal physiological function of this structure requires interaction and regulation by a variety of proteins, especially kinases...
April 13, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28400714/deletion-of-trpc6-attenuates-nmda-receptor-mediated-ca-2-entry-and-ca-2-induced-neurotoxicity-following-cerebral-ischemia-and-oxygen-glucose-deprivation
#13
Jin Chen, Zhaozhong Li, Jeffery T Hatcher, Qing-Hui Chen, Li Chen, Robert D Wurster, Sic L Chan, Zixi Cheng
Transient receptor potential canonical 6 (TRPC6) channels are permeable to Na(+) and Ca(2+) and are widely expressed in the brain. In this study, the role of TRPC6 was investigated following ischemia/reperfusion (I/R) and oxygen-glucose deprivation (OGD). We found that TRPC6 expression was increased in wild-type (WT) mice cortical neurons following I/R and in primary neurons with OGD, and that deletion of TRPC6 reduced the I/R-induced brain infarct in mice and the OGD- /neurotoxin-induced neuronal death. Using live-cell imaging to examine intracellular Ca(2+) levels ([Ca(2+)] i ), we found that OGD induced a significant higher increase in glutamate-evoked Ca(2+) influx compared to untreated control and such an increase was reduced by TRPC6 deletion...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28397127/a-novel-strategy-to-enhance-angiogenesis-in-vivo-using-the-small-vegf-binding-peptide-pr1p
#14
Avner Adini, Irit Adini, Zai-Long Chi, Ratmir Derda, Amy E Birsner, Benjamin D Matthews, Robert J D'Amato
Therapeutic angiogenesis is an experimental frontier in vascular biology that seeks to deliver angiogenic growth factors to ischemic or injured tissues to promote targeted formation of new blood vessels as an alternative approach to surgical revascularization procedures. Vascular endothelial growth factor (VEGF) is a potent angiogenic signal protein that is locally upregulated at sites of tissue injury. However, therapies aimed at increasing VEGF levels experimentally by injecting VEGF gene or protein failed to improve outcomes in human trials in part due to its short half-life and systemic toxicity...
April 10, 2017: Angiogenesis
https://www.readbyqxmd.com/read/28290048/carnosine-modulates-nitric-oxide-in-stimulated-murine-raw-264-7-macrophages
#15
Giuseppe Caruso, Claudia G Fresta, Francisco Martinez-Becerra, Lopalco Antonio, Ryan T Johnson, Richard P S de Campos, Joseph M Siegel, Manjula B Wijesinghe, Giuseppe Lazzarino, Susan M Lunte
Excess nitric oxide (NO) production occurs in several pathological states, including neurodegeneration, ischemia, and inflammation, and is generally accompanied by increased oxidative/nitrosative stress. Carnosine [β-alanine-histidine (β-Ala-His)] has been reported to decrease oxidative/nitrosative stress-associated cell damage by reducing the amount of NO produced. In this study, we evaluated the effect of carnosine on NO production by murine RAW 264.7 macrophages stimulated with lipopolysaccharides + interferon-γ...
March 13, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28272706/gc-ms-based-metabolomic-analysis-of-alleviated-renal-ischemia-reperfusion-injury-induced-by-remote-ischemic-preconditioning
#16
S Shen, J-F Wang, J-Q Wu, J-X Zhou, S-D Meng, J Ma, C -L Zhu, G-G Deng, D Liu
OBJECTIVE: Dysfunctional metabolisms have contributed towards ischemia-reperfusion (I/R) injury. However, the role of remote ischemic preconditioning (RIP) in I/R injury is not well known. The present study showed alleviated I/R injury in kidneys treated with RIP. MATERIALS AND METHODS: We utilized GC/MS-based metabolomics to characterize the variation of metabolomes. RESULTS: Metabolic category using differential metabolites showed the lower percentage of amino acids in I/R group in comparison to RIP+I/R group, confirming the importance of amino acid metabolism in RIP-treated rat kidney...
February 2017: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/28250763/molecular-chaperones-and-hypoxic-ischemic-encephalopathy
#17
REVIEW
Cong Hua, Wei-Na Ju, Hang Jin, Xin Sun, Gang Zhao
Hypoxic-ischemic encephalopathy (HIE) is a disease that occurs when the brain is subjected to hypoxia, resulting in neuronal death and neurological deficits, with a poor prognosis. The mechanisms underlying hypoxic-ischemic brain injury include excitatory amino acid release, cellular proteolysis, reactive oxygen species generation, nitric oxide synthesis, and inflammation. The molecular and cellular changes in HIE include protein misfolding, aggregation, and destruction of organelles. The apoptotic pathways activated by ischemia and hypoxia include the mitochondrial pathway, the extrinsic Fas receptor pathway, and the endoplasmic reticulum stress-induced pathway...
January 2017: Neural Regeneration Research
https://www.readbyqxmd.com/read/28210876/effect-of-hyperhomocysteinemia-on-redox-balance-and-redox-defence-enzymes-in-ischemia-reperfusion-injury-and-or-after-ischemic-preconditioning-in-rats
#18
Martin Petráš, Anna Drgová, Mária Kovalská, Zuzana Tatarková, Barbara Tóthová, Oľga Križanová, Ján Lehotský
Increased level of homocysteine (hHcy) in plasma is an accompanying phenomenon of many diseases, including a brain stroke. This study determines whether hyperhomocysteinemia (which is a risk factor of brain ischemia) itself or in combination with ischemic preconditioning affects the ischemia-induced neurodegenerative changes, generation of reactive oxygen species (ROS), lipoperoxidation, protein oxidation, and activity of antioxidant enzymes in the rat brain cortex. The hHcy was induced by subcutaneous administration of homocysteine (0...
February 16, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/28178567/defective-branched-chain-amino-acid-catabolism-disrupts-glucose-metabolism-and-sensitizes-the-heart-to-ischemia-reperfusion-injury
#19
Tao Li, Zhen Zhang, Stephen C Kolwicz, Lauren Abell, Nathan D Roe, Maengjo Kim, Bo Zhou, Yang Cao, Julia Ritterhoff, Haiwei Gu, Daniel Raftery, Haipeng Sun, Rong Tian
Elevated levels of branched-chain amino acids (BCAAs) have recently been implicated in the development of cardiovascular and metabolic diseases, but the molecular mechanisms are unknown. In a mouse model of impaired BCAA catabolism (knockout [KO]), we found that chronic accumulation of BCAAs suppressed glucose metabolism and sensitized the heart to ischemic injury. High levels of BCAAs selectively disrupted mitochondrial pyruvate utilization through inhibition of pyruvate dehydrogenase complex (PDH) activity...
February 7, 2017: Cell Metabolism
https://www.readbyqxmd.com/read/28164762/regulation-of-ion-channels-cellular-carriers-and-na-k-atpase-by-janus-kinase-3
#20
Mentor Sopjani, Shpëtim Thaçi, Berat Krasniqi, Miranda Selmonaj, Mark Rinnerthaler, Miribane Dërmaku-Sopjani
Janus kinase-3 (JAK3), a tyrosine kinase, is expressed in a variety of tissues, including the brain, and is involved in the signaling of cytokine receptors. JAK3 participates in numerous functions, among other the cell survival and proliferation, neuroprotection, apoptosis, as well as cellular response to hypoxia and ischemia-reperfusion. This kinase further contributes in the signaling of hematopoietic cell cytokine receptors, dendritic cells activation, maturation, and immune suppression as well as to cell volume regulation...
February 3, 2017: Current Medicinal Chemistry
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