Multiple-label immunocytochemistry for the evaluation of nature of cell death in experimental models of neurodegeneration

Adamec, Emil; Yang, Fusheng; Cole, Greg M.; Nixon, Ralph A.

doi:10.1016/s1385-299x(01)00072-1

Cited by 27 publications

(21 citation statements)

References 26 publications

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“…Intracere broventricular (ICV) injection of BDNF prior to HI injury almost completely abolished evidence of HI induced caspase3 activation in vivo. 10 In this study, astrocytes were no differences in the proportion of caspase3 activation among the nor moxia and 6 hr of hypoxia, but significant increase was shown between 18 hr of hypoxia and normoxia.…”

contrasting

confidence: 49%

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Brain-Derived Neurotrophic Factor (BDNF) Exerts a Protective Effect via an Anti-Apoptotic Mechanism on Hypoxic-Ischemic Injury in the Rat Brain

et al. 2016

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contrasting

confidence: 49%

“…9 Activated caspase3 is directly res ponsible for proteolytic cleavages of a variety of basic proteins involving cytoskeletal proteins, kinases, and DNArepair enzymes. 10 In addition to morphological evidence of apoptosis, Cheng et al (1998) 11 found evidence of delayed caspase3 activity following HI.…”

mentioning

confidence: 96%

Brain-Derived Neurotrophic Factor (BDNF) Exerts a Protective Effect via an Anti-Apoptotic Mechanism on Hypoxic-Ischemic Injury in the Rat Brain

et al. 2016

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“…Mouse primary neuronal cultures were prepared using standardized procedures as described elsewhere (2,32). SwissWebster mice at gestation day 16 were euthanized, and the embryos were removed.…”

Section: Methodsmentioning

confidence: 99%

Attenuated Rabies Virus Activates, while Pathogenic Rabies Virus Evades, the Host Innate Immune Responses in the Central Nervous System

Wang¹,

Sarmento²,

Wang

et al. 2005

J Virol

212

203

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Rabies virus (RV) induces encephalomyelitis in humans and animals. However, the pathogenic mechanism of rabies is not fully understood. To investigate the host responses to RV infection, we examined and compared the pathology, particularly the inflammatory responses, and the gene expression profiles in the brains of mice infected with wild-type (wt) virus silver-haired bat RV (SHBRV) or laboratory-adapted virus B2C, using a mouse genomic array (Affymetrix). Extensive inflammatory responses were observed in animals infected with the attenuated RV, but little or no inflammatory responses were found in mice infected with wt RV. Furthermore, attenuated RV induced the expression of the genes involved in the innate immune and antiviral responses, especially those related to the alpha/beta interferon (IFN-␣/␤) signaling pathways and inflammatory chemokines. For the IFN-␣/␤ signaling pathways, many of the interferon regulatory genes, such as the signal transduction activation transducers and interferon regulatory factors, as well as the effector genes, for example, 2-5-oligoadenylate synthetase and myxovirus proteins, are highly induced in mice infected with attenuated RV. However, many of these genes were not up-regulated in mice infected with wt SHBRV. The data obtained by microarray analysis were confirmed by real-time PCR. Together, these data suggest that attenuated RV activates, while pathogenic RV evades, the host innate immune and antiviral responses.Rabies virus (RV) is a nonsegmented negative-stranded RNA virus of the Rhabdoviridae family and induces a fatal neurological disease in humans and animals (15). Although significant advances have been made in rabies prevention and control, the disease remains a major threat to public health and continues to cause numerous human deaths around the world. The dog remains the most important reservoir in Asia, Africa, and Latin America, where most human rabies cases occur (19). In the United States, dog rabies has been largely brought under control through pet vaccination programs, and there have been only a few incidents where large carnivores have transmitted rabies directly to humans (11,26). Most of the human cases in the past decade have been associated with RV found in bats, particularly silver-haired bats (11,18,39,47). Furthermore, most of the cases occurred without a history of exposure (11), suggesting that the silver-haired bat RV (SHBRV) is highly pathogenic and neuroinvasive (18,47).RV invades the nervous system by binding to neural receptors, such as acetylcholine receptor (31), neural cell adhesion molecule (52), or nerve growth factor receptor (NTR75) (53). Then, RV is transported to the central nervous system (CNS) by retrograde transportation, possibly by binding to cytoplasmic dynein (29,46). Despite extensive investigation in the past 100 years, the pathogenic mechanisms by which street (wildtype [wt]) RV infection results in neurological diseases and death in humans are not well understood. This is because there is very little neuronal pathology or d...

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“…To investigate this, we quantified total numbers of degenerated neurons and only counted cells fulfilling the morphological criteria of neuronal degeneration, as defined by fragmented neuronal processes, cell shrinkage, and somatic swelling. 47 Quantification revealed significant increases in neuronal degeneration after exposing primary neurons to ferucarbotran (all concentrations; Figure 3B-D), VSOP-R2 (1.5 mM and 3.0 mM; Figure 3C and D) and ferumoxytol (1.5 mM; Figure 3C). In contrast to primary microglia (Figure 2) …”

Section: Primary Hippocampal Neurons Degenerate After Spio Exposurementioning

confidence: 96%

“…Neurons were classified as degenerated according to standard morphological criteria, ie, fragmentation of neuronal processes, cell shrinkage, and somatic swelling. 47 Quantification of neurons was performed via double determination of three independently prepared primary neuron cultures and four independently prepared neuron-glia cocultures for each exposure condition (see Table 3 for sample size and total number of measurements).…”

Section: Quantification and Analysis Of Primary Hippocampal Neuronsmentioning

confidence: 99%

New findings about iron oxide nanoparticles and their different effects on murine primary brain cells

Neubert¹,

Wagner²,

Kiwit³

et al. 2015

IJN

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The physicochemical properties of superparamagnetic iron oxide nanoparticles (SPIOs) enable their application in the diagnostics and therapy of central nervous system diseases. However, since crucial information regarding side effects of particle–cell interactions within the central nervous system is still lacking, we investigated the influence of novel very small iron oxide particles or the clinically approved ferucarbotran or ferumoxytol on the vitality and morphology of brain cells. We exposed primary cell cultures of microglia and hippocampal neurons, as well as neuron–glia cocultures to varying concentrations of SPIOs for 6 and/or 24 hours, respectively. Here, we show that SPIO accumulation by microglia and subsequent morphological alterations strongly depend on the respective nanoparticle type. Microglial viability was severely compromised by high SPIO concentrations, except in the case of ferumoxytol. While ferumoxytol did not cause immediate microglial death, it induced severe morphological alterations and increased degeneration of primary neurons. Additionally, primary neurons clearly degenerated after very small iron oxide particle and ferucarbotran exposure. In neuron–glia cocultures, SPIOs rather stimulated the outgrowth of neuronal processes in a concentration- and particle-dependent manner. We conclude that the influence of SPIOs on brain cells not only depends on the particle type but also on the physiological system they are applied to.

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Multiple-label immunocytochemistry for the evaluation of nature of cell death in experimental models of neurodegeneration

Cited by 27 publications

References 26 publications

Brain-Derived Neurotrophic Factor (BDNF) Exerts a Protective Effect via an Anti-Apoptotic Mechanism on Hypoxic-Ischemic Injury in the Rat Brain

Brain-Derived Neurotrophic Factor (BDNF) Exerts a Protective Effect via an Anti-Apoptotic Mechanism on Hypoxic-Ischemic Injury in the Rat Brain

Attenuated Rabies Virus Activates, while Pathogenic Rabies Virus Evades, the Host Innate Immune Responses in the Central Nervous System

New findings about iron oxide nanoparticles and their different effects on murine primary brain cells

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Multiple-label immunocytochemistry for the evaluation of nature of cell death in experimental models of neurodegeneration

Cited by 27 publications

References 26 publications

Brain-Derived Neurotrophic Factor (BDNF) Exerts a Protective Effect via an Anti-Apoptotic Mechanism on Hypoxic-Ischemic Injury in the Rat Brain

Brain-Derived Neurotrophic Factor (BDNF) Exerts a Protective Effect via an Anti-Apoptotic Mechanism on Hypoxic-Ischemic Injury in the Rat Brain

Attenuated Rabies Virus Activates, while Pathogenic Rabies Virus Evades, the Host Innate Immune Responses in the Central Nervous System

New findings about iron oxide nanoparticles and&nbsp;their different effects on murine primary brain cells

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New findings about iron oxide nanoparticles and their different effects on murine primary brain cells