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  • 1
    Online Resource
    Online Resource
    Overexpression of CuZn superoxide dismutase protects RAW 264.7 macrophages against nitric oxide cytotoxicity
    Portland Press Ltd. ; 1999
    In:  Biochemical Journal Vol. 338, No. 2 ( 1999-03-01), p. 295-303
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 338, No. 2 ( 1999-03-01), p. 295-303
    Abstract: Initiation of nitric oxide (NO•)-mediated apoptotic cell death in RAW 264.7 macrophages is associated with up-regulation of mitochondrial manganese superoxide dismutase (MnSOD; SOD2) and down-regulation of cytosolic copper zinc superoxide dismutase (CuZnSOD; SOD1) at their individual mRNA and protein levels. To evaluate the decreased CuZnSOD expression and the initiation of apoptosis we stably transfected macrophages to overexpress human CuZnSOD. Individual clones revealed a 2-fold increase in CuZnSOD activity. Expression of a functional and thus protective CuZnSOD was verified by attenuated superoxide (O2•-)-mediated apoptotic as well as necrotic cell death. In this study we showed that SOD-overexpressing macrophages (R-SOD1-12) were also protected against NO•-initiated programmed cell death. Protection was substantial towards NO• derived from exogenously added NO donors or when NO• was generated by inducible NO synthase activation, and was evident at the level of p53 accumulation, caspase activation and DNA fragmentation. Stimulation of parent and SOD-overexpressing cells with a combination of lipopolysaccharide and murine interferon γ produced equivalent amounts of nitrite/nitrate, which ruled out attenuated inducible NO• synthase activity during protection. Because protection by a O2•--scavenging system during NO•-intoxication implies a role of NO• and O2•- in the progression of cell damage, we used uric acid to delineate the role of peroxynitrite during NO•-elicited apoptosis. The peroxynitrite scavenger uric acid left S-nitrosoglutathione or spermine-NO-elicited apoptosis unaltered, blocking only 3-morpholinosydnonimine-mediated cell death. As a result we exclude peroxynitrite from contributing, to any major extent, to NO•-mediated apoptosis. Therefore protection observed with CuZnSOD overexpression is unlikely to stem from interference with peroxynitrite formation and/or action. Unequivocally, the down-regulation of CuZnSOD is associated with NO• cytotoxicity, whereas CuZnSOD overexpression protects macrophages from apoptosis.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj3380295
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1999
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    p300 relieves p53-evoked transcriptional repression of hypoxia-inducible factor-1 (HIF-1)
    Portland Press Ltd. ; 2004
    In:  Biochemical Journal Vol. 380, No. 1 ( 2004-05-15), p. 289-295
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 380, No. 1 ( 2004-05-15), p. 289-295
    Abstract: HIF-1 (hypoxia-inducible factor-1), a heterodimeric transcription factor comprising HIF-1α and HIF-1β subunits, serves as a key regulator of metabolic adaptation to hypoxia. HIF-1 activity largely increases during hypoxia by attenuating pVHL (von Hippel–Lindau protein)-dependent ubiquitination and subsequent 26 S-proteasomal degradation of HIF-1α. Besides HIF-1, the transcription factor and tumour suppressor p53 accumulates and is activated under conditions of prolonged/severe hypoxia. Recently, the interaction between p53 and HIF-1α was reported to evoke HIF-1α degradation. Destruction of HIF-1α by p53 was corroborated in the present study by using pVHL-deficient RCC4 (renal carcinoma) cells, supporting the notion of a pVHL-independent degradation process. In addition, low p53 expression repressed HIF-1 transactivation without affecting HIF-1α protein amount. Establishing that p53-evoked inhibition of HIF-1 reporter activity was relieved upon co-transfection of p300 suggested competition between p53 and HIF-1 for limiting amounts of the shared co-activator p300. This assumption was confirmed by showing competitive binding of in vitro transcription/translation-generated p53 and HIF-1α to the CH1 domain of p300 in vitro. We conclude that low p53 expression attenuates HIF-1 transactivation by competing for p300, whereas high p53 expression destroys the HIF-1α protein and thereby eliminates HIF-1 reporter activity. Thus once p53 becomes activated under conditions of severe hypoxia/anoxia, it contributes to terminating HIF-1 responses.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj20031299
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2004
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Heat shock proteins and macrophage resistance to the toxic effects of nitric oxide
    Portland Press Ltd. ; 1996
    In:  Biochemical Journal Vol. 315, No. 3 ( 1996-05-01), p. 845-849
    Details
    In: Biochemical Journal, Portland Press Ltd., Vol. 315, No. 3 ( 1996-05-01), p. 845-849
    Abstract: Nitric oxide (NO) functions as a pathophysiological mediator in mammalian tissues. Activated macrophages produce NO as a non-specific immune response directed against invading bacteria or micro-organisms. The same macrophages that initiate the production of NO also can be toxically affected by NO. Incubation of RAW 264.7 macrophages with lipopolysaccharide (LPS) and/or interferon-γ (INF-γ) induced the formation of NO by the activation of a cytokine-inducible NO synthase (NOS). The viability of these macrophages was inversely correlated with the formation of nitrite, a final NO-oxidation product measurable in the incubation medium. The addition of an NOS inhibitor, NG-monomethyl-L-arginine, diminished NO formation and preserved cell viability in a dose- and time-dependent fashion. Treatment of macrophages with ten cycles of non-lethal doses of LPS and INF-γ, each followed by subculturing of the surviving cells, resulted in cell resistance to the NO toxic insult induced by LPS and INF-γ. These resistant macrophages showed a 2-fold increase in the expression of the constitutive heat shock protein (HSC 70) which is known to be involved in protecting cells against the action of various metabolic insults. Our results establish a link between cell resistance to the toxic effects of NO, and the expression of heat shock proteins in RAW 264.7 macrophages.
    Type of Medium: Online Resource
    ISSN: 0264-6021 , 1470-8728
    URL: Article
    DOI: 10.1042/bj3150845
    RVK:
    WA 15000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 1996
    detail.hit.zdb_id: 1473095-9
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Loss of cardiac mitochondrial complex I persulfidation impairs NAD+ homeostasis in aging
    Elsevier BV ; 2024
    In:  Redox Biology Vol. 69 ( 2024-02), p. 103014-
    Details
    In: Redox Biology, Elsevier BV, Vol. 69 ( 2024-02), p. 103014-
    Type of Medium: Online Resource
    ISSN: 2213-2317
    URL: Article
    DOI: 10.1016/j.redox.2023.103014
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2024
    detail.hit.zdb_id: 2701011-9
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  • 5
    Online Resource
    Online Resource
    Necrosis in DU145 prostate cancer spheroids induces COX‐2/mPGES‐1‐derived PGE 2 to promote tumor growth and to inhibit T cell activation
    Wiley ; 2013
    In:  International Journal of Cancer Vol. 133, No. 7 ( 2013-10), p. 1578-1588
    Details
    In: International Journal of Cancer, Wiley, Vol. 133, No. 7 ( 2013-10), p. 1578-1588
    Abstract: What's new? Prostaglandin E2 (PGE2) helps cancers grow, but stopping the COX‐2 pathway that produces it, without generating harmful side effects, has been challenging. In this paper, the authors looked at the effects of blocking the enzyme microsomal PGE synthase 1 (mPGES‐1). Previous experiments have returned mixed reports of whether mPGES‐1 boosts tumors. The authors employed the technique of growing tumor cells in multicellular tumor spheroids (MCTS), which better mimics the condition of growth within a living organism than growing them in suspension. They found that while lack of mPGES‐1 didn't faze tumor cells grown in monolayer, it did slow the growth of the MCTS, indicating that tumors growing within an animal probably depend on the enzyme.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v133.7
    DOI: 10.1002/ijc.28181
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2013
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 6
    Online Resource
    Online Resource
    Ebselen affects calcium homeostasis in human platelets
    Elsevier BV ; 1991
    In:  Biochemical Pharmacology Vol. 41, No. 12 ( 1991-06), p. 1805-1811
    Details
    In: Biochemical Pharmacology, Elsevier BV, Vol. 41, No. 12 ( 1991-06), p. 1805-1811
    Type of Medium: Online Resource
    ISSN: 0006-2952
    URL: Article
    DOI: 10.1016/0006-2952(91)90118-O
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1991
    detail.hit.zdb_id: 1496199-4
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    miR-193a-3p increases glycolysis under hypoxia by facilitating Akt phosphorylation and PFKFB3 activation in human macrophages
    Springer Science and Business Media LLC ; 2022
    In:  Cellular and Molecular Life Sciences Vol. 79, No. 2 ( 2022-02)
    Details
    In: Cellular and Molecular Life Sciences, Springer Science and Business Media LLC, Vol. 79, No. 2 ( 2022-02)
    Abstract: Human macrophages infiltrating hypoxic regions alter their metabolism, because oxygen becomes limited. Increased glycolysis is one of the most common cellular adaptations to hypoxia and mostly is regulated via hypoxia-inducible factor (HIF) and RAC-alpha serine/threonine–protein kinase (Akt) signaling, which gets activated under reduced oxygen content. We noticed that micro RNA (miR)-193a-3p enhances Akt phosphorylation at threonine 308 under hypoxia. In detail, miR-193a-3p suppresses the protein abundance of phosphatase PTC7 homolog (PPTC7), which in turn increases Akt phosphorylation. Lowering PPTC7 expression by siRNA or overexpressing miR-193a-3p increases Akt phosphorylation. Vice versa, inhibition of miR-193a-3p attenuates Akt activation and prevents a subsequent increase of glycolysis under hypoxia. Excluding effects of miR-193a-3p and Akt on HIF expression, stabilization, and function, we noticed phosphorylation of 6 phosphofructo-2-kinase/fructose 2,6-bisphosphatase PFKFB3 in response to the PI3K/Akt/mTOR signaling cascade. Inhibition of PFKFB3 blocked an increased glycolytic flux under hypoxia. Apparently, miR-193a-3p balances Akt phosphorylation and dephosphorylation by affecting PPTC7 protein amount. Suppression of PPTC7 increases Akt activation and phosphorylation of PFKFB3, which culminates in higher rates of glycolysis under hypoxia.
    Type of Medium: Online Resource
    ISSN: 1420-682X , 1420-9071
    URL: Article
    DOI: 10.1007/s00018-022-04146-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 1458497-9
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Nitric oxide and its role in apoptosis
    Elsevier BV ; 1998
    In:  European Journal of Pharmacology Vol. 351, No. 3 ( 1998-6), p. 261-272
    Details
    In: European Journal of Pharmacology, Elsevier BV, Vol. 351, No. 3 ( 1998-6), p. 261-272
    Type of Medium: Online Resource
    ISSN: 0014-2999
    URL: Article
    DOI: 10.1016/S0014-2999(98)00274-X
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1998
    detail.hit.zdb_id: 1483526-5
    SSG: 15,3
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  • 9
    Online Resource
    Online Resource
    Mesangial cells but not hepatocytes are protected against NO/O2− cogeneration: mechanistic considerations
    Elsevier BV ; 2002
    In:  European Journal of Pharmacology Vol. 444, No. 1-2 ( 2002-5), p. 1-11
    Details
    In: European Journal of Pharmacology, Elsevier BV, Vol. 444, No. 1-2 ( 2002-5), p. 1-11
    Type of Medium: Online Resource
    ISSN: 0014-2999
    URL: Article
    DOI: 10.1016/S0014-2999(02)01555-8
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2002
    detail.hit.zdb_id: 1483526-5
    SSG: 15,3
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  • 10
    Online Resource
    Online Resource
    NO-Evoked Macrophage Apoptosis Is Attenuated by cAMP-Induced Gene Expression
    Springer Science and Business Media LLC ; 1999
    In:  Molecular Medicine Vol. 5, No. 10 ( 1999-10), p. 672-684
    Details
    In: Molecular Medicine, Springer Science and Business Media LLC, Vol. 5, No. 10 ( 1999-10), p. 672-684
    Type of Medium: Online Resource
    ISSN: 1076-1551 , 1528-3658
    URL: Article
    DOI: 10.1007/BF03401986
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1999
    detail.hit.zdb_id: 1475577-4
    detail.hit.zdb_id: 1283676-X
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