Guy C Brown

Summary

Affiliation: University of Cambridge
Country: UK

Publications

  1. ncbi Cell biology. NO says yes to mitochondria
    Guy C Brown
    Department of Biochemistry, Cambridge University, Cambridge CB2 1QW, UK
    Science 299:838-9. 2003
  2. ncbi Nitric oxide and mitochondria
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, United Kingdom
    Front Biosci 12:1024-33. 2007
  3. doi Eaten alive! Cell death by primary phagocytosis: 'phagoptosis'
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Trends Biochem Sci 37:325-32. 2012
  4. pmc Nitric oxide protects the heart from ischemia-induced apoptosis and mitochondrial damage via protein kinase G mediated blockage of permeability transition and cytochrome c release
    Vilmante Borutaite
    Institute for Biomedical Research, Kaunas University of Medicine, Kaunas, Lithuania
    J Biomed Sci 16:70. 2009
  5. ncbi Nitric oxide, mitochondria, and cell death
    G C Brown
    Department of Biochemistry, University of Cambridge, United Kingdom
    IUBMB Life 52:189-95. 2001
  6. ncbi Mechanisms of inflammatory neurodegeneration: iNOS and NADPH oxidase
    G C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, U K
    Biochem Soc Trans 35:1119-21. 2007
  7. ncbi Interactions between nitric oxide, oxygen, reactive oxygen species and reactive nitrogen species
    G C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochem Soc Trans 34:953-6. 2006
  8. ncbi Nitric oxide inhibition of mitochondrial respiration and its role in cell death
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom
    Free Radic Biol Med 33:1440-50. 2002
  9. ncbi Inflammatory neurodegeneration mediated by nitric oxide, glutamate, and mitochondria
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Mol Neurobiol 27:325-55. 2003
  10. ncbi Inhibition of mitochondrial respiratory complex I by nitric oxide, peroxynitrite and S-nitrosothiols
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochim Biophys Acta 1658:44-9. 2004

Collaborators

Detail Information

Publications63

  1. ncbi Cell biology. NO says yes to mitochondria
    Guy C Brown
    Department of Biochemistry, Cambridge University, Cambridge CB2 1QW, UK
    Science 299:838-9. 2003
  2. ncbi Nitric oxide and mitochondria
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, United Kingdom
    Front Biosci 12:1024-33. 2007
    ..Reactive nitrogen species activation of the mitochondrial permeability transition pore may cause apoptosis or necrosis. NO may protect against mitochondria-mediated cell death by multiple mechanisms...
  3. doi Eaten alive! Cell death by primary phagocytosis: 'phagoptosis'
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Trends Biochem Sci 37:325-32. 2012
    ..This review provides an overview of the molecular signals that regulate phagoptosis and the physiological and pathological circumstances in which it has been observed...
  4. pmc Nitric oxide protects the heart from ischemia-induced apoptosis and mitochondrial damage via protein kinase G mediated blockage of permeability transition and cytochrome c release
    Vilmante Borutaite
    Institute for Biomedical Research, Kaunas University of Medicine, Kaunas, Lithuania
    J Biomed Sci 16:70. 2009
    ..We tested whether nitric oxide (NO) can block this damage in isolated rat heart, and, if so, by what mechanisms...
  5. ncbi Nitric oxide, mitochondria, and cell death
    G C Brown
    Department of Biochemistry, University of Cambridge, United Kingdom
    IUBMB Life 52:189-95. 2001
    ....
  6. ncbi Mechanisms of inflammatory neurodegeneration: iNOS and NADPH oxidase
    G C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, U K
    Biochem Soc Trans 35:1119-21. 2007
    ..Activation of PHOX alone causes no death, but when combined with expressed iNOS results in extensive neuronal death via peroxynitrite production...
  7. ncbi Interactions between nitric oxide, oxygen, reactive oxygen species and reactive nitrogen species
    G C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochem Soc Trans 34:953-6. 2006
    ..This review briefly describes the main interactions between ROS and RNS and shows how their origins, chemistry, metabolism and biological actions are intimately linked...
  8. ncbi Nitric oxide inhibition of mitochondrial respiration and its role in cell death
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom
    Free Radic Biol Med 33:1440-50. 2002
    ..However, NO can induce (and inhibit) cell death by a variety of mechanisms unrelated to respiratory inhibition...
  9. ncbi Inflammatory neurodegeneration mediated by nitric oxide, glutamate, and mitochondria
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Mol Neurobiol 27:325-55. 2003
    ....
  10. ncbi Inhibition of mitochondrial respiratory complex I by nitric oxide, peroxynitrite and S-nitrosothiols
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochim Biophys Acta 1658:44-9. 2004
    ..Inactivation of complex I by NO or RNS is seen in cells or tissues expressing iNOS, and may be relevant to inflammatory pathologies, such as septic shock and Parkinson's disease...
  11. doi Inflammatory neurodegeneration and mechanisms of microglial killing of neurons
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QW, UK
    Mol Neurobiol 41:242-7. 2010
    ..Finally, microglial phagocytosis of these stressed neurons may contribute to their loss...
  12. doi Nitric oxide and neuronal death
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, United Kingdom
    Nitric Oxide 23:153-65. 2010
    ..iNOS is induced in glia by inflammation, and may protect; however, if there is also hypoxia or the NADPH oxidase is active, it can induce neuronal death. Microglial phagocytosis may contribute actively to neuronal loss...
  13. ncbi Transcellular regulation of cell respiration by nitric oxide generated by activated macrophages
    G C Brown
    Department of Biochemistry, University of Cambridge, UK
    FEBS Lett 439:321-4. 1998
    ..Thus, NO generated by one cell can regulate the respiration of adjacent cells, supporting the hypothesis that NO may be a physiological and/or pathological regulator of cellular respiration, via its inhibition of cytochrome oxidase...
  14. ncbi Nitric oxide and mitochondrial respiration
    G C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochim Biophys Acta 1411:351-69. 1999
    ..Mitochondrial damage by peroxynitrite may mediate the cytotoxicity of NO, and may be involved in a variety of pathologies...
  15. ncbi Nitric oxide and mitochondrial respiration in the heart
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Cardiovasc Res 75:283-90. 2007
    ..NO inhibition of mitochondrial respiration is likely to be more important in the heart during hypoxia and/or pathologies where iNOS is expressed...
  16. ncbi Spatial gradients of cellular phospho-proteins
    G C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambrigde, UK
    FEBS Lett 457:452-4. 1999
    ..The estimated gradients of phospho-proteins were potentially very large, which has important implications for cellular signalling...
  17. ncbi Regulation of mitochondrial respiration by nitric oxide inhibition of cytochrome c oxidase
    G C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochim Biophys Acta 1504:46-57. 2001
    ..Thus the NO inhibition of cytochrome oxidase may be involved in the physiological and/or pathological regulation of respiration rate, and its affinity for oxygen...
  18. doi The principle of sufficiency and the evolution of control: using control analysis to understand the design principles of biological systems
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochem Soc Trans 38:1210-4. 2010
    ..Thus in an optimized system small changes in parameters will have a negligible effect on fitness. This principle naturally leads to (and is supported by) the dominance of wild-type alleles over null mutants...
  19. pmc MFG-E8 mediates primary phagocytosis of viable neurons during neuroinflammation
    Michael Fricker
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, UK
    J Neurosci 32:2657-66. 2012
    ..Our data show that blocking MFG-E8-dependent phagocytosis preserves live neurons, implying that phagocytosis actively contributes to neuronal death during brain inflammation...
  20. ncbi Nitric oxide from inflammatory-activated glia synergizes with hypoxia to induce neuronal death
    Palwinder Mander
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, United Kingdom
    J Neurosci Res 79:208-15. 2005
    ..Brain inflammation can thus sensitize to hypoxia-induced death, which may be important in pathologies such as stroke, neurodegeneration, and brain aging...
  21. pmc Phagocytosis executes delayed neuronal death after focal brain ischemia
    Jonas J Neher
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom
    Proc Natl Acad Sci U S A 110:E4098-107. 2013
    ..Therefore, inhibition of specific phagocytic pathways may present therapeutic targets for preventing delayed neuronal loss after transient cerebral ischemia. ..
  22. ncbi Nitric oxide from inducible nitric oxide synthase sensitizes the inflamed aorta to hypoxic damage via respiratory inhibition
    Vilmante Borutaite
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom
    Shock 23:319-23. 2005
    ..This NO-induced sensitization of aorta to mild hypoxia may be important in sepsis and other pathologies where iNOS is expressed...
  23. ncbi Nitric oxide from neuronal nitric oxide synthase sensitises neurons to hypoxia-induced death via competitive inhibition of cytochrome oxidase
    Aiste Jekabsone
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    J Neurochem 103:346-56. 2007
    ..These data indicate that hypoxia synergises with NO from nNOS to induce neuronal death via cytochrome oxidase inhibition causing neuronal depolarisation. This mechanism might contribute to ischaemia/stroke-induced neuronal death in vivo...
  24. doi Inhibition of microglial phagocytosis is sufficient to prevent inflammatory neuronal death
    Jonas J Neher
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom
    J Immunol 186:4973-83. 2011
    ..Thus, blocking phagocytosis may prevent some forms of inflammatory neurodegeneration, and therefore might be beneficial during brain infection, trauma, ischemia, neurodegeneration, and aging...
  25. ncbi Nitric oxide stimulates PC12 cell proliferation via cGMP and inhibits at higher concentrations mainly via energy depletion
    Anna Bal-Price
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge, UK
    Nitric Oxide 14:238-46. 2006
    ..Our results indicate that NO at low concentrations increases cell proliferation via cGMP, while high concentrations of NO block proliferation via inhibition of both glycolysis and respiration, causing energy depletion...
  26. ncbi Nitric oxide induces apoptosis via hydrogen peroxide, but necrosis via energy and thiol depletion
    Vilmante Borutaite
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    Free Radic Biol Med 35:1457-68. 2003
    ..We conclude that: (i). NO-induced apoptosis is mediated by H(2)O(2); (ii). NO-induced necrosis is mediated by energy failure speeded by thiol depletion...
  27. ncbi Nitric oxide induces rapid, calcium-dependent release of vesicular glutamate and ATP from cultured rat astrocytes
    Anna Bal-Price
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    Glia 40:312-23. 2002
    ..NO-induced release of astrocytic glutamate and ATP may be important in physiological or pathological communication between astrocytes and neurons...
  28. pmc Primary phagocytosis of viable neurons by microglia activated with LPS or Aβ is dependent on calreticulin/LRP phagocytic signalling
    Michael Fricker
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QW, UK
    J Neuroinflammation 9:196. 2012
    ..Calreticulin (CRT) exposure on the surface of cancer cells can promote their phagocytosis via LRP (low-density lipoprotein receptor-related protein) on macrophages, but it is not known whether this occurs with neurons and microglia...
  29. pmc Caspase inhibitors protect neurons by enabling selective necroptosis of inflamed microglia
    Michael Fricker
    Department of Biochemistry, University of Cambridge, Cambridge, CB2 1QW, United Kingdom
    J Biol Chem 288:9145-52. 2013
    ..We conclude that the activation of caspase-8 in inflamed microglia prevents their death by necroptosis, and thus, caspase-8 inhibitors may protect neurons in the inflamed brain by selectively killing activated microglia...
  30. ncbi Nitric oxide-induced cell death of cerebrocortical murine astrocytes is mediated through p53- and Bax-dependent pathways
    Hong Wa Yung
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    J Neurochem 89:812-21. 2004
    ..More generally, our data suggest that apoptotic mediators should be evaluated as the cause of cell death even in cases where a full apoptotic phenotype is lacking...
  31. ncbi S-nitrosothiol inhibition of mitochondrial complex I causes a reversible increase in mitochondrial hydrogen peroxide production
    Vilmante Borutaite
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochim Biophys Acta 1757:562-6. 2006
    ..The results suggest that S-nitrosation of complex I can reversibly increase oxidant production by mitochondria, which is potentially important in cell signalling and/or pathology...
  32. pmc Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia
    Urte Neniskyte
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom
    J Biol Chem 286:39904-13. 2011
    ..Inhibition of phagocytosis prevented neuronal loss with no increase in neuronal death, even after 7 days, suggesting that microglial phagocytosis was the primary cause of neuronal death induced by nanomolar Aβ...
  33. doi Lactadherin/MFG-E8 is essential for microglia-mediated neuronal loss and phagoptosis induced by amyloid β
    Urte Neniskyte
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    J Neurochem 126:312-7. 2013
    ..The essential role of MFG-E8 in Aβ-induced phagoptosis, suggests this bridging protein as a potential therapeutic target to prevent neuronal loss in Alzheimer's disease. ..
  34. ncbi Stimulation of the NADPH oxidase in activated rat microglia removes nitric oxide but induces peroxynitrite production
    Anna Bal-Price
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB1 2QW, UK
    J Neurochem 80:73-80. 2002
    ..Thus, microglial NADPH oxidase can regulate the bioavailability of NO and the production of peroxynitrite...
  35. ncbi Arachidonate and NADPH oxidase synergise with iNOS to induce death in macrophages: mechanisms of inflammatory degeneration
    Vilmante Borutaite
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Pharmacol Rep 58:96-102. 2006
    ....
  36. ncbi Different pathways for iNOS-mediated toxicity in vitro dependent on neuronal maturation and NMDA receptor expression
    Sabine Golde
    Cambridge Centre for Brain Repair, University of Cambridge, Cambridge, UK
    J Neurochem 82:269-82. 2002
    ..Our results therefore extend existing evidence for NO-mediated toxicity and show a complex interaction between inflammatory and excitotoxic mechanisms of injury in mature neurones...
  37. doi Rotenone induces neuronal death by microglial phagocytosis of neurons
    Julius V Emmrich
    Department of Biochemistry, University of Cambridge, UK
    FEBS J 280:5030-8. 2013
    ..Thus, neuronal loss in Parkinson's disease and other neurological diseases might be prevented by blocking phagocytic signalling...
  38. ncbi Microglia proliferation is regulated by hydrogen peroxide from NADPH oxidase
    Palwinder K Mander
    Department of Biochemistry, University of Cambridge, Cambridge, United Kingdom
    J Immunol 176:1046-52. 2006
    ..In conclusion, these findings indicate that microglial proliferation in response to IL-1beta or TNF-alpha is mediated by hydrogen peroxide from NADPH oxidase...
  39. ncbi Inhibition of mitochondrial permeability transition prevents mitochondrial dysfunction, cytochrome c release and apoptosis induced by heart ischemia
    Vilmante Borutaite
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    J Mol Cell Cardiol 35:357-66. 2003
    ..The MPT-induced cytochrome c release is also largely responsible for the ischemic respiratory inhibition, which might contribute to contractile dysfunction or necrosis at reperfusion...
  40. doi Dependence of leukemic cell proliferation and survival on H2O2 and L-arginine
    Richard D Brown
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    Free Radic Biol Med 46:1211-20. 2009
    ..Arginase, H(2)O(2), ascorbic acid, and ebselen might be useful in the treatment of leukemia...
  41. doi Regulation of apoptosis by the redox state of cytochrome c
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochim Biophys Acta 1777:877-81. 2008
    ..Regulation of the redox state of cytochrome c potentially enables regulation of the intrinsic pathway of apoptosis at a relatively late stage...
  42. ncbi Mitochondria in apoptosis of ischemic heart
    Vilmante Borutaite
    Department of Biochemistry, University of Cambridge, UK
    FEBS Lett 541:1-5. 2003
    ..Cytochrome c release can result in caspase activation and thus apoptosis, but also results in mitochondrial dysfunction, which might contribute to contractile dysfunction or necrosis at reperfusion...
  43. ncbi Nitric oxide donors, nitrosothiols and mitochondrial respiration inhibitors induce caspase activation by different mechanisms
    V Borutaite
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge, UK
    FEBS Lett 467:155-9. 2000
    ....
  44. ncbi Nitric-oxide-induced necrosis and apoptosis in PC12 cells mediated by mitochondria
    A Bal-Price
    Department of Biochemistry, University of Cambridge, Cambridge, England
    J Neurochem 75:1455-64. 2000
    ..Further, our results indicate that the mode of cell death (necrosis versus apoptosis) induced by either NO or mitochondrial inhibitors depends critically on the glycolytic capacity of the cell...
  45. ncbi Release of cytochrome c from heart mitochondria is induced by high Ca2+ and peroxynitrite and is responsible for Ca(2+)-induced inhibition of substrate oxidation
    V Borutaite
    Institute for Biomedical Research, Kaunas Medical University, Lithuania
    Biochim Biophys Acta 1453:41-8. 1999
    ....
  46. ncbi Caspases are reversibly inactivated by hydrogen peroxide
    V Borutaite
    Department of Biochemistry, University of Cambridge, Downing Site, Tennis Court Road, CB2 1QW, Cambridge, UK
    FEBS Lett 500:114-8. 2001
    ..Activation of H2O2-producing NADPH oxidase in macrophages also caused catalase-sensitive inactivation of cellular caspases. The data suggest that the activity of caspases in cells can be directly but reversibly inhibited by H2O2...
  47. ncbi Inflammatory neurodegeneration mediated by nitric oxide from activated glia-inhibiting neuronal respiration, causing glutamate release and excitotoxicity
    A Bal-Price
    Department of Biochemistry, University of Cambridge, Cambridge, CB2 1QW, United Kingdom
    J Neurosci 21:6480-91. 2001
    ..This may contribute to neuronal cell death in inflammatory, infectious, ischemic, and neurodegenerative diseases...
  48. ncbi Release of mitochondrial cytochrome c and activation of cytosolic caspases induced by myocardial ischaemia
    V Borutaite
    Department of Biochemistry, University of Cambridge, UK
    Biochim Biophys Acta 1537:101-9. 2001
    ..Our data suggest that extended heart ischaemia can cause apoptosis mediated by release of cytochrome c from mitochondria and subsequent activation of caspase-3...
  49. pmc The NO donor DETA-NONOate reversibly activates an inward current in neurones and is not mediated by the released nitric oxide
    A J Thompson
    Department of Biochemistry, University of Cambridge, Cambridge, UK
    Br J Pharmacol 158:1338-43. 2009
    ..It has been previously shown that high levels of nitric oxide (NO), from NO donors, kill neurones, but the mechanisms are unclear...
  50. ncbi Reversible inhibition of cellular respiration by nitric oxide in vascular inflammation
    V Borutaite
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, United Kingdom
    Am J Physiol Heart Circ Physiol 281:H2256-60. 2001
    ..These results suggest that during inflammation and sepsis, tissue respiration may be substantially reduced due to inhibition by NO of cytochrome oxidase...
  51. ncbi Nitric oxide, hypoxia and brain inflammation
    P Mander
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochem Soc Trans 32:1068-9. 2004
    ..Thus the NO from neuronal NOS during excitotoxicity or the NO from inducible NOS during inflammation may sensitize the brain to hypoxic/ischaemic damage...
  52. ncbi Activated human neutrophils rapidly break down nitric oxide
    A G McBride
    Department of Biochemistry, University of Cambridge, UK
    FEBS Lett 417:231-4. 1997
    ..These results suggest that activation of human neutrophils in vivo will dramatically decrease surrounding NO levels, potentially causing vasoconstriction, platelet aggregation and adhesion and peroxynitrite (ONOO-) formation...
  53. ncbi Neurodegeneration in models of Gram-positive bacterial infections of the central nervous system
    J J Neher
    Department of Biochemistry, University of Cambridge, Downing Site, Tennis Court Road, Cambridge CB2 1QW, U K
    Biochem Soc Trans 35:1166-7. 2007
    ..LTA-activated microglia kill co-cultured neurons apparently via nitric oxide, superoxide and peroxynitrite, which may induce apoptosis of neurons that are then phagocytosed by microglia...
  54. ncbi Superoxide dismutase and hydrogen peroxide cause rapid nitric oxide breakdown, peroxynitrite production and subsequent cell death
    A G McBride
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Biochim Biophys Acta 1454:275-88. 1999
    ....
  55. doi There is no evidence that mitochondria are the main source of reactive oxygen species in mammalian cells
    Guy C Brown
    Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK
    Mitochondrion 12:1-4. 2012
    ..Mitochondria can rapidly degrade ROS and thus are potential sinks for ROS, but whether mitochondria act as net sources or sinks within cells in particular conditions is unknown...
  56. pmc Primary phagocytosis of neurons by inflamed microglia: potential roles in neurodegeneration
    Jonas J Neher
    Department of Biochemistry, University of Cambridge Cambridge, UK
    Front Pharmacol 3:27. 2012
    ..In this review, we discuss the mechanisms of phagocytic cell death and its potential roles in Alzheimer's Disease, Parkinson's Disease, and Frontotemporal Dementia...
  57. pmc Tetramethylphenylenediamine protects the isolated heart against ischaemia-induced apoptosis and reperfusion-induced necrosis
    Jurgita Barauskaite
    Institute for Biomedical Research, Lithuanian University of Health Sciences, Kaunas, Lithuania
    Br J Pharmacol 162:1136-42. 2011
    ....
  58. doi Analysis of microglial production of reactive oxygen and nitrogen species
    Urte Neniskyte
    University of Cambridge, Cambridge, UK
    Methods Mol Biol 1041:103-11. 2013
    ..Here we describe quick methods to assess the production of superoxide, hydrogen peroxide, nitric oxide, and peroxynitrite by microglia...
  59. ncbi Inflammatory neurodegeneration induced by lipoteichoic acid from Staphylococcus aureus is mediated by glia activation, nitrosative and oxidative stress, and caspase activation
    Agnieszka Kinsner
    European Centre for the Validation of Alternative Methods ECVAM, European Commission Joint Research Centre, Ispra, Italy
    J Neurochem 95:1132-43. 2005
    ....
  60. ncbi Nitric oxide and calcium together inactivate mitochondrial complex I and induce cytochrome c release
    Aiste Jekabsone
    Institute for Biomedical Research, Kaunas University of Medicine, Eiveniu 4, LT 3007, Kaunas, Lithuania
    J Mol Cell Cardiol 35:803-9. 2003
    ..Thus, NO and calcium appear to synergistically inhibit mitochondrial respiration, partly by inactivation of complex I and partly by inducing cytochrome c release...
  61. ncbi Highly purified lipoteichoic acid induced pro-inflammatory signalling in primary culture of rat microglia through Toll-like receptor 2: selective potentiation of nitric oxide production by muramyl dipeptide
    Agnieszka Kinsner
    European Centre for the Validation of Alternative Methods, ECVAM, European Commission Joint Research Centre, Ispra, VA, Italy
    J Neurochem 99:596-607. 2006
    ..The observed pro-inflammatory response induced by lipoteichoic acid-activated microglia could play a major role in the inflammatory response of CNS induced by Gram-positive bacteria...
  62. ncbi S-nitrosothiol-induced rapid cytochrome c release, caspase activation and mitochondrial permeability transition in perfused heart
    Aiste Jekabsone
    Institute for Biomedical Research, Kaunas University of Medicine, Kaunas, Lithuania
    Biochem Pharmacol 66:1513-9. 2003
    ..These data suggest that S-nitrosothiols are potent inducers of apoptosis in the heart and that S-nitrosothiol-induced apoptosis is mediated by mitochondrial permeability transition but not via NO...
  63. ncbi Mitochondrial regulation of caspase activation by cytochrome oxidase and tetramethylphenylenediamine via cytosolic cytochrome c redox state
    Vilmante Borutaite
    Institute for Biomedical Research, Kaunas University of Medicine, Eiveniu 4, Kaunas LT 50009, Lithuania
    J Biol Chem 282:31124-30. 2007
    ..However, this activation can be blocked by adding TMPD, which may have some therapeutic potential...