Molecular stress response in the CNS of mice after systemic exposure to interferon-α, ionizing radiation and ketamine

Lowe, Xiu; Marchetti, Francesco; Lü, Xing; Wyrobek, Andrew J.

doi:10.1016/j.neuro.2008.12.012

Cited by 13 publications

(17 citation statements)

References 48 publications

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“…The consistency of finding the TP53, MYC and FOS nodes across human and mouse tissues (Table 5) and their broadly associated functions (Table 4) suggest that there are significantly conserved biological response functions after low dose exposures. In a recent study, we have also shown a strong concordance between signaling pathways that are down regulated in the mouse brain and those that are down regulated with normal human aging and in patients with Alzheimer's diseases [81].…”

Section: Mechanisms and Implicationsmentioning

confidence: 55%

Low dose radiation response curves, networks and pathways in human lymphoblastoid cells exposed from 1 to 10cGy of acute gamma radiation

Wyrobek

Manohar

Krishnan

et al. 2011

Mutation Research/Genetic Toxicology and Environmental Mutagene

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We investigated the low dose dependency of the transcriptional response of human cells to characterize the shape and biological functions associated with the dose response curve and to identify common and conserved functions of low dose expressed genes across cells and tissues.Human lymphoblastoid (HL) cells from two unrelated individuals were exposed to graded doses of radiation spanning the range of 1-10 cGy were analyzed by transcriptome profiling, qPCR and bioinformatics, in comparison to sham irradiated samples. A set of ~80 genes showed consistent responses in both cell lines; these genes were associated with homeostasis mechanisms (e.g., membrane signaling, molecule transport), subcellular locations (e.g., Golgi, and endoplasmic reticulum), and involved diverse signal transduction pathways. The majority of radiation-modulated genes had plateau-like responses across 1-10 cGy, some with suggestive evidence that transcription was modulated at doses below 1 cGy. MYC, FOS and TP53 were the major network nodes of the low-dose response in HL cells. Comparison our low dose expression findings in HL cells with those of prior studies in mouse brain after whole body exposure, in human keratinocyte cultures, and in endothelial cells cultures, indicates that certain components of the low dose radiation response are broadly conserved across cell types and tissues, independent of proliferation status.

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Section: Mechanisms and Implicationsmentioning

confidence: 55%

Low dose radiation response curves, networks and pathways in human lymphoblastoid cells exposed from 1 to 10cGy of acute gamma radiation

Wyrobek

Manohar

Krishnan

et al. 2011

Mutation Research/Genetic Toxicology and Environmental Mutagene

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“…Similar brain damage and impaired cognition were observed following exposure to 100 mGy of γ irradiation [41, 42]. …”

Section: Ldir and Ldrir-induced Bionegative Effects In Animal Modelsmentioning

confidence: 68%

“…At 3 months post irradiation, decrease in neurogenesis was still observable following 500 mGy irradiation [40]. Similar brain damage and impaired cognition were observed following exposure to 100 mGy of γ irradiation [41, 42]. …”

Section: Ldir and Ldrir-induced Bionegative Effects In Animal Modelsmentioning

confidence: 95%

Low-dose or low-dose-rate ionizing radiation–induced bioeffects in animal models

Tang

Loke

Khoo

2016

Journal of Radiation Research

117

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Animal experimental studies indicate that acute or chronic low-dose ionizing radiation (LDIR) (≤100 mSv) or low-dose-rate ionizing radiation (LDRIR) (<6 mSv/h) exposures may be harmful. It induces genetic and epigenetic changes and is associated with a range of physiological disturbances that includes altered immune system, abnormal brain development with resultant cognitive impairment, cataractogenesis, abnormal embryonic development, circulatory diseases, weight gain, premature menopause in female animals, tumorigenesis and shortened lifespan. Paternal or prenatal LDIR/LDRIR exposure is associated with reduced fertility and number of live fetuses, and transgenerational genomic aberrations. On the other hand, in some experimental studies, LDIR/LDRIR exposure has also been reported to bring about beneficial effects such as reduction in tumorigenesis, prolonged lifespan and enhanced fertility. The differences in reported effects of LDIR/LDRIR exposure are dependent on animal genetic background (susceptibility), age (prenatal or postnatal days), sex, nature of radiation exposure (i.e. acute, fractionated or chronic radiation exposure), type of radiation, combination of radiation with other toxic agents (such as smoking, pesticides or other chemical toxins) or animal experimental designs. In this review paper, we aimed to update radiation researchers and radiologists on the current progress achieved in understanding the LDIR/LDRIR-induced bionegative and biopositive effects reported in the various animal models. The roles played by a variety of molecules that are implicated in LDIR/LDRIR-induced health effects will be elaborated. The review will help in future investigations of LDIR/LDRIR-induced health effects by providing clues for designing improved animal research models in order to clarify the current controversial/contradictory findings from existing studies.

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“…The neurological deficits of high-dose radiation are progressively detrimental over time and are thought to be due to demyelination and neural loss with associated neural and cognitive deficiencies. Some of these cognitive defects have been observed as a consequence of impaired neurogenesis after exposure to IR [49]. …”

Section: Effects Of Ionizing Radiation On the Brainmentioning

confidence: 99%

“…There is no shortage of studies describing gene modulations resulting from exposure to IR at various doses in a number of experimental models [70–73], including in the brain [9, 49, 74]. A recent study has shown that exposure to low doses of IR trigger gene modulations that are different from those triggered by high doses and involve genes associated with damage response functions (such as those controlled by Trp53 and Myc) and brain-specific functions, such as memory, learning and cognition [9].…”

Section: Effects Of Ionizing Radiation On the Brainmentioning

confidence: 99%

Does ionizing radiation influence Alzheimer's disease risk?

Begum

Wang²,

Mori³

et al. 2012

Journal of Radiation Research

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Alzheimer's disease (AD) is a human neurodegenerative disease, and its global prevalence is predicted to increase dramatically in the following decades. There is mounting evidence describing the effects of ionizing radiation (IR) on the brain, suggesting that exposure to IR might ultimately favor the development of AD. Therefore better understanding the possible connections between exposure to IR and AD pathogenesis is of utmost importance. In this review, recent developments in the research on the biological and cognitive effects of IR in the brain will be explored. Because AD is largely an age-related pathology, the effects of IR on ageing will be investigated.

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Molecular stress response in the CNS of mice after systemic exposure to interferon-α, ionizing radiation and ketamine

Cited by 13 publications

References 48 publications

Low dose radiation response curves, networks and pathways in human lymphoblastoid cells exposed from 1 to 10cGy of acute gamma radiation

Low dose radiation response curves, networks and pathways in human lymphoblastoid cells exposed from 1 to 10cGy of acute gamma radiation

Low-dose or low-dose-rate ionizing radiation–induced bioeffects in animal models

Does ionizing radiation influence Alzheimer's disease risk?

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