Ultrastructural localization of heme oxygenase-1 to the neurofibrillary pathology of Alzheimer disease

Smith, Mark A.; Richey, Peggy L.; Kutty, R. Krishnan; Wiggert, Barbara; Perry, George

doi:10.1007/bf02962147

Cited by 163 publications

(213 citation statements)

References 5 publications

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“…Oxidative stress also induces haem oxygenase, and this can be used as a marker for stressed cells (Smith et al, 1994). The ex vivo tumour stained positive for both markers (Figure 4).…”

Section: Resultsmentioning

confidence: 99%

Cooperative stimulation of vascular endothelial growth factor expression by hypoxia and reactive oxygen species: the effect of targeting vascular endothelial growth factor and oxidative stress in an orthotopic xenograft model of bladder carcinoma

et al. 2005

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Elevated thymidine phosphorylase has been shown to correlate with increased angiogenesis and poor prognosis in many cancers including transitional cell carcinoma of the bladder. In vitro studies have demonstrated that thymidine phosphorylase activity causes cellular oxidative stress and increases secretion of vascular endothelial growth factor. In this study, we show that thymidine phosphorylase activity also augments levels of the hypoxia-inducible factor-1a during in vitro hypoxia, and that thymidine phosphorylase activity and hypoxia act in concert to increase vascular endothelial growth factor (VEGF) secretion. We also demonstrate that thymidine phosphorylase overexpression confers tumorigenicity on an orthotopically implanted transitional cell carcinoma cell line. Administration of the antioxidant N-acetylcysteine together with a blocking anti-VEGF antibody abrogates the increase in tumorigenicity. Our results support the increased efficacy of combination approaches to antiangiogenic therapy.

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“…Oxidative stress also induces haem oxygenase, and this can be used as a marker for stressed cells (Smith et al, 1994). The ex vivo tumour stained positive for both markers (Figure 4).…”

Section: Resultsmentioning

confidence: 99%

Cooperative stimulation of vascular endothelial growth factor expression by hypoxia and reactive oxygen species: the effect of targeting vascular endothelial growth factor and oxidative stress in an orthotopic xenograft model of bladder carcinoma

et al. 2005

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“…Physiologically, ROS are found in all aerobic organisms and arise from the secondary production of superoxide by mitochondrial reduction of molecular oxygen, the production of H 2 O 2 by oxidases such as monoamine oxidase, and the reaction of superoxide with nitric oxide to yield peroxynitrite, which is capable of both oxidation and nitration reactions. The hydroxyl radical is the principal ROS implicated in biologically relevant oxidative stress and is responsible, either directly or indirectly, for most of the free radical damage seen in AD [12][13][14][15][16]. In mice with accelerated senescence, several of the processes associated with mitochondrial dysfunction have been shown to lead [35] to a vicious circle with the formation of more free radicals resulting in neuronal disturbances [17][18][19][20], as shown in Table 1.…”

Section: First Steps In Characterizing Samp8mentioning

confidence: 99%

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Pallàs

2012

ISRN Cell Biology

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The causes of aging remain unknown, but they are probably intimately linked to a multifactorial process that affects cell networks to varying degrees. Although a growing number of aging and Alzheimer's disease (AD) animal models are available, a more comprehensive and physiological mouse model is required. In this context, the senescence-accelerated mouse prone 8 (SAMP8) has a number of advantages, since its rapid physiological senescence means that it has about half the normal lifespan of a rodent. In addition, according to data gathered over the last five years, some of its behavioral traits and histopathology resemble AD human dementia. SAMP8 has remarkable pathological similarities to AD and may prove to be an excellent model for acquiring more in-depth knowledge of the age-related neurodegenerative processes behind brain senescence and AD in particular. We review these facts and particularly the data on parameters related to neurodegeneration. SAMP8 also shows signs of aging in the immune, vascular, and metabolic systems, among others.

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“…This suggests that neuroinflammatory cytokines may be one of the known toxicants including beta-amyloid (Cotman & Su, 1996;Square, 1997;Matsukawa et al ., 2002), presenilins (Cotman & Su, 1996;Furukawa et al ., 1998;Hashimoto et al ., 2002) and free radicals (Smith et al ., 1992(Smith et al ., , 1994Carney & Carney, 1994;Hensley et al ., 1996;Joseph et al ., 1998;McCann et al ., 1998;Butterfield et al ., 1999;Kaufmann et al ., 2001) involved in the neuronal impairments characterizing central nervous system (CNS) aging and the progression of associated diseases. TNF α acts through specific receptors (TNFR-I and TNFR-II) that can positively activate a dual signalling cascade that in different cell types may lead to apoptosis, proliferation, differentiation or survival (Gruss, 1996;Arch et al ., 1998;Orlinick & Chao, 1998;Macdonald et al ., 2000).…”

Section: Introductionmentioning

confidence: 99%

Tumour necrosis factor‐alpha‐ vs. growth factor deprivation‐promoted cell death: distinct converging pathways

et al. 2003

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SummaryPerturbations of neuronal physiological homeostasis are likely to underscore neuronal demise/impairments that are reportedly associated with aging of the central nervous system and age-related neurodegenerative diseases such as Alzheimer's disease (AD). A number of ageand/or disease-associated neurotoxic events has been described. These include abnormally modified proteins such as beta amyloid and hyper-phosphorylated Tau, cytokines such as tumour necrosis factor-alpha (TNFα α α α ), high levels of free radicals conducive to oxidative stress, and impaired/decreased neuronal trophic support by neurotrophic factors. Overall, it could be argued that toxic events in the aged brain are either active, such as those due to a direct action of cytokines, or passive, such as those due to lack of growth factor support. It is therefore conceivable that cellular responses to such diverse toxic stimuli are different, suggesting that interventions should be targeted accordingly. In order to begin answering this question, we determined in PC12 cells the time course of activity, in response to TNFα α α α (active) or growth factor withdrawal (passive), of protein kinase c-zeta (PKCζ ζ ζ ζ ), nuclear factor kappa B (NFκ κ κ κ B), caspases 3 and 8, and poly (ADP-ribose) polymerase (PARP), key signal transduction elements associated with modulation of cell death/survival in PC12 cells. We found that the overall activity of PKCζ ζ ζ ζ , NFκ κ κ κ B and caspase 8 was significantly different depending on the apoptotic initiator. The pattern of caspase 3 and PARP activity, however, was not statistically different between serum-free-and TNFα α α α -induced cell death conditions. This suggests that two distinct cell responses are elicited that converge at caspase 3, which then induces downstream events involved in the execution of a common apoptotic programme. These results contribute to the aim of differentially targeting neuronal death in the aged brain (characterized by neurotrophic factor impairments) or in the diseased brain (e.g. AD, characterized by elevated levels of pro-inflammatory cytokines).

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Ultrastructural localization of heme oxygenase-1 to the neurofibrillary pathology of Alzheimer disease

Cited by 163 publications

References 5 publications

Cooperative stimulation of vascular endothelial growth factor expression by hypoxia and reactive oxygen species: the effect of targeting vascular endothelial growth factor and oxidative stress in an orthotopic xenograft model of bladder carcinoma

Cooperative stimulation of vascular endothelial growth factor expression by hypoxia and reactive oxygen species: the effect of targeting vascular endothelial growth factor and oxidative stress in an orthotopic xenograft model of bladder carcinoma

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Tumour necrosis factor‐alpha‐ vs. growth factor deprivation‐promoted cell death: distinct converging pathways

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