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Chapter by: Klein, Catherine B.; Costa, Max
in: Handbook on the Toxicology of Metals by
[S.l.] : Elsevier Inc., 2021
pp. 615-637
ISBN: 9780128229460
CID: 5189482

Launching the "Projections" series in mutation research reviews with a special issue on next generation sequencing [Editorial]

Klein, Catherine B; Parsons, Barbara L
PMID: 34893159
ISSN: 1388-2139
CID: 5107812

ToxPoint: Using Multiomics to Bridge the Gap Between Electronic Cigarette Research and Disease Etiology

Avenbuan, Oyemwenosa N; Klein, Catherine B; Zelikoff, Judith T
PMID: 33259631
ISSN: 1096-0929
CID: 4734842

Passing of the pen: Editorship of Mutation Research - Reviews in Mutation Research [Editorial]

Parsons, Barbara L; Klein, Catherine B
PMID: 32192647
ISSN: 1873-135x
CID: 4353702

Formaldehyde, Epigenetics, and Alzheimer's Disease

Wang, Fei; Chen, Danqi; Wu, Peipei; Klein, Catherine; Jin, Chunyuan
Alzheimer's disease (AD) is the most common form of dementia. The accumulation of β-amyloid plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau protein are two hallmarks of AD. The β-amyloid and tau proteins have been at the center of AD research and drug development for decades. However, most of the clinical trials targeting β-amyloid have failed. Whereas the safety and efficacy of most tau-targeting drugs have not yet been completely assessed, the first tau aggregation inhibitor, LMTX, failed in a late-stage trial, leading to further recognition of the complexities of AD and reconsideration of the amyloid hypothesis and perhaps the tau hypothesis as well. Multilevel complex interactions between genetic, epigenetic, and environmental factors contribute to the occurrence and progression of AD. Formaldehyde (FA) is a widespread environmental organic pollutant. It is also an endogenous metabolite in the human body. Recent studies suggest that elevation of FA in the body by endogenous and/or exogenous exposure may play important roles in AD development. We have demonstrated that FA reduces lysine acetylation of cytosolic histones, thereby compromising chromatin assembly and resulting in the loss of histone content in chromatin, a conserved feature of aging from yeast to humans. Aging is an important factor for AD progression. Therefore, FA-induced inhibition of chromatin assembly and the loss of histones may contribute to AD initiation and/or development. This review will briefly summarize current knowledge on mechanistic insights into AD, focusing on epigenetic alterations and the involvement of FA in AD development. The exploration of chemical exposures as contributing factors to AD may provide new insights into AD mechanisms and could identify potential novel therapeutic targets.
PMID: 30964647
ISSN: 1520-5010
CID: 3903242

Emerging confluences of epigenetics and DNA repair in cancer and disease [Editorial]

Klein, Catherine B
PMID: 31395354
ISSN: 1873-135x
CID: 4034442

EMGS-50 living history project [Meeting Abstract]

Van, Gijssel H E; Klein, C B
During the 2017 annual EMGS meeting awards ceremony, background information was shared about the person who served as the inspiration for one of these awards: Alexander Hollaender. Afterwards, people would tell us their stories about the founding of the EMGS and their personal memories of Alexander Hollaender. Some members who were involved with the founding of the EMGS, as well as members who interacted with Alexander Hollaender, are still active within EMGS. It is therefore important to collect and archive these stories, not only to archive the history of EMGS, but also to perpetuate the historical and continued excitement in the field. Therefore, the " EMGS 50 - Living History" project was created. The purpose of the project is to collect stories/memories from any member of the society. This project is modelled after the NPR StoryCorps' project, such that video stories will be collected for the EMGS history project. These stories will be published, with other relevant documents, on a timeline on the EMGS website, to create an interactive " living" history document of the EMGS. The goal of the project is to create at least one video for every year since EMGS began. This project is financially supported by the EMGS Endowment Fund and approved by the EMGS executive board. Inaugural videos will be collected during the 2018 the annual meeting and will serve as the basis for the 50th Anniversary symposium at the 50th Annual Meeting in Washington DC in 2019. Please join us in the video recording area and share your memories with EMGS. Instructions will be provided
ISSN: 1098-2280
CID: 3331222

Microglia Activation and Gene Expression Alteration of Neurotrophins in the Hippocampus Following Early Life Exposure to E-cigarette Aerosols in a Murine Model

Zelikoff, Judith T; Parmalee, Nancy; Corbett, Kevin; Gordon, Terry; Klein, Catherine B; Aschner, Michael
Recent epidemiological data indicate that the popularity of electronic cigarettes (e-cigarettes), and consequently nicotine use, is rising in both adolescent and adult populations. As nicotine is a known developmental neurotoxin, these products present a potential threat for those exposed during early life stages. Despite this, few studies have evaluated the toxicity of e-cigarettes on the developing central nervous system (CNS). The goal of this study was to assess neurotoxicity resulting from early life exposure to electronic cigarette aerosols in an in vivo model. Specifically, studies here focused on neuro-parameters related to neuroinflammation and neurotrophins. To accomplish this, pregnant and neonatal C57BL/6 mice were exposed to aerosols produced from classic tobacco flavor e-cigarette cartridges (with [13 mg/ml] and without nicotine) during gestation ( approximately 3-wk) and lactation ( approximately 3-wk) via whole-body inhalation. Exposure to e-cigarette aerosols with and without nicotine caused significant reductions in hippocampal gene expression of Ngfr and Bdnf, as well as in serum levels of cytokines IL-1beta, IL-2 and IL-6. Exposure to e-cigarette aerosols without nicotine enhanced expression of Iba-1, a specific marker of microglia, in the CA1 region of the hippocampus. Overall, our novel results indicate that exposure to e-cigarette aerosols, with and without nicotine, poses a considerable risk to the developing CNS. Consequently, e-cigarettes should be considered a potential public health threat, especially early in life, requiring further research and policy considerations.
PMID: 29161446
ISSN: 1096-0929
CID: 2792372

Looking at the Environmental Mutagenesis and Genomics Society Through the Lens of Bibliometric Data Analysis: Identifying Relationships and Areas for Growth [Meeting Abstract]

Weston, EH; Mantooth, SN; Knight, EN; Klein, CB; Ward, JB; Banda, M; Nicolette, JJ; Smith-Roe, SL
ISSN: 1098-2280
CID: 2696122

Frontal Cortex Transcriptome Analysis of Mice Exposed to Electronic Cigarettes During Early Life Stages

Lauterstein, Dana E; Tijerina, Pamella B; Corbett, Kevin; Akgol Oksuz, Betul; Shen, Steven S; Gordon, Terry; Klein, Catherine B; Zelikoff, Judith T
Electronic cigarettes (e-cigarettes), battery-powered devices containing nicotine, glycerin, propylene glycol, flavorings, and other substances, are increasing in popularity. They pose a potential threat to the developing brain, as nicotine is a known neurotoxicant. We hypothesized that exposure to e-cigarettes during early life stages induce changes in central nervous system (CNS) transcriptome associated with adverse neurobiological outcomes and long-term disease states. To test the hypothesis, pregnant C57BL/6 mice were exposed daily (via whole body inhalation) throughout gestation (3 h/day; 5 days/week) to aerosols produced from e-cigarettes either with nicotine (13-16 mg/mL) or without nicotine; following birth, pups and dams were exposed together to e-cigarette aerosols throughout lactation beginning at postnatal day (PND) 4-6 and using the same exposure conditions employed during gestational exposure. Following exposure, frontal cortex recovered from ~one-month-old male and female offspring were excised and analyzed for gene expression by RNA Sequencing (RNA-Seq). Comparisons between the treatment groups revealed that e-cigarette constituents other than nicotine might be partly responsible for the observed biological effects. Transcriptome alterations in both offspring sexes and treatment groups were all significantly associated with downstream adverse neurobiological outcomes. Results from this study demonstrate that e-cigarette exposure during early life alters CNS development potentially leading to chronic neuropathology.
PMID: 27077873
ISSN: 1660-4601
CID: 2078432