Joel Meyer

Overview:

Dr. Meyer studies the effects of toxic agents and stressors on human and wildlife health. He is particularly interested in understanding the mechanisms by which environmental agents cause DNA damage, the molecular processes that organisms employ to protect prevent and repair DNA damage, and genetic differences that may lead to increased or decreased sensitivity to DNA damage. Mitochondrial DNA damage and repair, as well as mitochondrial function in general, are a particular focus. He studies these effects in the nematode Caenorhabditis elegans, in cell culture, and collaboratively in other laboratory model organisms as well as in human populations in the USA and globally.

Positions:

Truman and Nellie Semans/Alex Brown and Sons Associate Professor of Molecular Environmental Toxicology

Environmental Sciences and Policy
Nicholas School of the Environment

Associate Professor of Environmental Genomics in the Division of Environmental Sciences and Policy

Environmental Sciences and Policy
Nicholas School of the Environment

Associate Professor in the Department of Civil and Environmental Engineering

Civil and Environmental Engineering
Pratt School of Engineering

Faculty Network Member of The Energy Initiative

Duke University Energy Initiative
Institutes and Provost's Academic Units

Affiliate, Duke Global Health Institute

Duke Global Health Institute
Institutes and Provost's Academic Units

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 1992

Juniata College

Ph.D. 2003

Duke University

Grants:

Center for Environmental Implications of Nanotechnology

Administered By
Pratt School of Engineering
Awarded By
National Science Foundation
Role
Investigator
Start Date
End Date

Fluoride and human health: Assessing novel biomarkers in detecting bone disorder

Administered By
Earth and Climate Sciences
Awarded By
National Institutes of Health
Role
Collaborator
Start Date
End Date

COPAS BIOSORT Worm Sorter

Administered By
Neurology, Headache and Pain
Awarded By
National Institutes of Health
Role
Collaborator
Start Date
End Date

Are mitochondria a major target of antimicrobial silver nanoparticles?

Administered By
Environmental Sciences and Policy
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

GW150184 Mitochondrial dysfunction and Gulf War Illness

Administered By
Environmental Sciences and Policy
Awarded By
United States Army Medical Research Acquisition Activity
Role
Principal Investigator
Start Date
End Date

Publications:

Multiple metabolic changes mediate the response of Caenorhabditis elegans to the complex I inhibitor rotenone.

Rotenone, a mitochondrial complex I inhibitor, has been widely used to study the effects of mitochondrial dysfunction on dopaminergic neurons in the context of Parkinson's disease. Although the deleterious effects of rotenone are well documented, we found that young adult Caenorhabditis elegans showed resistance to 24 and 48 h rotenone exposures. To better understand the response to rotenone in C. elegans, we evaluated mitochondrial bioenergetic parameters after 24 and 48 h exposures to 1 μM or 5 μM rotenone. Results suggested upregulation of mitochondrial complexes II and V following rotenone exposure, without major changes in oxygen consumption or steady-state ATP levels after rotenone treatment at the tested concentrations. We found evidence that the glyoxylate pathway (an alternate pathway not present in higher metazoans) was induced by rotenone exposure; gene expression measurements showed increases in mRNA levels for two complex II subunits and for isocitrate lyase, the key glyoxylate pathway enzyme. Targeted metabolomics analyses showed alterations in the levels of organic acids, amino acids, and acylcarnitines, consistent with the metabolic restructuring of cellular bioenergetic pathways including activation of complex II, the glyoxylate pathway, glycolysis, and fatty acid oxidation. This expanded understanding of how C. elegans responds metabolically to complex I inhibition via multiple bioenergetic adaptations, including the glyoxylate pathway, will be useful in interrogating the effects of mitochondrial and bioenergetic stressors and toxicants.
Authors
Gonzalez-Hunt, CP; Luz, AL; Ryde, IT; Turner, EA; Ilkayeva, OR; Bhatt, DP; Hirschey, MD; Meyer, JN
MLA Citation
Gonzalez-Hunt, Claudia P., et al. “Multiple metabolic changes mediate the response of Caenorhabditis elegans to the complex I inhibitor rotenone.Toxicology, vol. 447, Jan. 2021, p. 152630. Pubmed, doi:10.1016/j.tox.2020.152630.
URI
https://scholars.duke.edu/individual/pub1465328
PMID
33188857
Source
pubmed
Published In
Toxicology
Volume
447
Published Date
Start Page
152630
DOI
10.1016/j.tox.2020.152630

Analysis of Illumina 450K DNA Methylation in NEST Cord Blood Reveals Sex Differences at Mitochondrial Genes in the Nuclear Genome.

Authors
King, D; Martinez, M; Lloyd, D; Maguire, R; Hoyo, C; Meyer, JN; Murphy, SK
MLA Citation
King, D., et al. “Analysis of Illumina 450K DNA Methylation in NEST Cord Blood Reveals Sex Differences at Mitochondrial Genes in the Nuclear Genome.Environmental and Molecular Mutagenesis, vol. 61, 2020, pp. 34–35.
URI
https://scholars.duke.edu/individual/pub1467214
Source
wos-lite
Published In
Environmental and Molecular Mutagenesis
Volume
61
Published Date
Start Page
34
End Page
35

Evaluation of Peruvian Government Interventions to Reduce Childhood Anemia.

<h4>Background</h4>In Peru, anemia has been a persistent health problem that is known to lead to irreversible cognitive and developmental deficits in children. The Peruvian government has recently made anemia a primary health concern by passing legislation in 2017 that makes anemia an intersectoral priority. This new legislation fortifies previous programs while creating new programs that target specific age groups.<h4>Objectives</h4>Evaluate the effectiveness of government programs in Madre de Dios, Peru to reduce anemia prevalence and increase hemoglobin levels among children ages 2-11 years old.<h4>Methods</h4>Propensity scores are used to match 688 children enrolled in 2018, after the legislation, and 2,140 children enrolled in previous studies our team conducted in the region between 2014 and 2017, based on sex, age (years), intervention status (prior/post), community income, presence of a health post in the community (yes/no), community type (indigenous, non-indigenous rural, non-indigenous urban) and road access (fraction of the number of months out of the year with road access). A pseudo matched case-control analysis to evaluate changes in anemia prevalence and hemoglobin was conducted using t-tests and multivariate models. Program effectiveness is evaluated overall, by age groups (2-4, 5-7 and 8-11 years old), and community type (indigenous vs. urban).<h4>Findings</h4>The adjusted odds ratio indicated lower odds of anemia (OR = 0.31, 95%CI 0.17-0.54) for children exposed to the anemia prevention programs vs. those not exposed. The effect was not significantly different across age groups; however, the intervention effects significantly differed by community type among children 8-11 years old, with urban children less likely to benefit from anemia interventions (OR = 0.69, 95% CI 0.38-1.25) compared to indigenous children (OR = 0.21, 95% CI 0.08-0.56).<h4>Conclusion</h4>Government programs to reduce anemia in Madre de Dios were found to be associated with reduced anemia prevalence in the study communities. However, the lack of program monitoring precludes the attribution of anemia decline to specific interventions or program components. In addition, regional anemia prevalence remains high according to the 2019 Demographic and Health Survey, suggesting impaired population impact. Program monitoring and evaluation is a key component of health interventions to improve program implementation effectiveness.
Authors
Berky, AJ; Robie, E; Ortiz, EJ; Meyer, JN; Hsu-Kim, H; Pan, WK
MLA Citation
Berky, Axel J., et al. “Evaluation of Peruvian Government Interventions to Reduce Childhood Anemia.Annals of Global Health, vol. 86, no. 1, Aug. 2020, p. 98. Epmc, doi:10.5334/aogh.2896.
URI
https://scholars.duke.edu/individual/pub1457432
PMID
32864350
Source
epmc
Published In
Annals of Global Health
Volume
86
Published Date
Start Page
98
DOI
10.5334/aogh.2896

Risuteganib Protects against Hydroquinone-induced Injury in Human RPE Cells.

Purpose: Cigarette smoking has been implicated in the pathogenesis of AMD. Integrin dysfunctions have been associated with AMD. Herein, we investigate the effect of risuteganib (RSG), an integrin regulator, on RPE cell injury induced by hydroquinone (HQ), an important oxidant in cigarette smoke. Methods: Cultured human RPE cells were treated with HQ in the presence or absence of RSG. Cell death, mitochondrial respiration, reactive oxygen species production, and mitochondrial membrane potential were measured by flow cytometry, XFe24 analyzer, and fluorescence plate reader, respectively. Whole transcriptome analysis and gene expression were analyzed by Illumina RNA sequencing and quantitative PCR, respectively. F-actin aggregation was visualized with phalloidin. Levels of heme oxygenase-1, P38, and heat shock protein 27 proteins were measured by Western blot. Results: HQ induced necrosis and apoptosis, decreased mitochondrial bioenergetics, increased reactive oxygen species levels, decreased mitochondrial membrane potential, increased F-actin aggregates, and induced phosphorylation of P38 and heat shock protein 27. HQ, but not RSG alone, induced substantial transcriptome changes that were regulated by RSG cotreatment. RSG cotreatment significantly protected against HQ-induced necrosis and apoptosis, prevented HQ-reduced mitochondrial bioenergetics, decreased HQ-induced reactive oxygen species production, improved HQ-disrupted mitochondrial membrane potential, reduced F-actin aggregates, decreased phosphorylation of P38 and heat shock protein 27, and further upregulated HQ-induced heme oxygenase-1 protein levels. Conclusions: RSG has no detectable adverse effects on healthy RPE cells, whereas RSG cotreatment protects against HQ-induced injury, mitochondrial dysfunction, and actin reorganization, suggesting a potential role for RSG therapy to treat retinal diseases such as AMD.
Authors
Yang, P; Shao, Z; Besley, NA; Neal, SE; Buehne, KL; Park, J; Karageozian, H; Karageozian, V; Ryde, IT; Meyer, JN; Jaffe, GJ
MLA Citation
Yang, Ping, et al. “Risuteganib Protects against Hydroquinone-induced Injury in Human RPE Cells.Invest Ophthalmol Vis Sci, vol. 61, no. 10, Aug. 2020, p. 35. Pubmed, doi:10.1167/iovs.61.10.35.
URI
https://scholars.duke.edu/individual/pub1456316
PMID
32818234
Source
pubmed
Published In
Investigative Opthalmology & Visual Science
Volume
61
Published Date
Start Page
35
DOI
10.1167/iovs.61.10.35

Characterizing The Bioenergetic Profile Of White Blood Cells For Utility In Assessing Mitochondrial Dysfunction In Gulf War Illness

Authors
Alexander, T; Falvo, MJ; Ryde, I; Klein-Adams, J; Ndirangu, DS; Watson, M; Qian, W; Eager, NA; Condon, M; Meyer, JN
MLA Citation
Alexander, Thomas, et al. “Characterizing The Bioenergetic Profile Of White Blood Cells For Utility In Assessing Mitochondrial Dysfunction In Gulf War Illness.” Medicine and Science in Sports and Exercise, vol. 52, no. 17, 2020, pp. 302–302.
URI
https://scholars.duke.edu/individual/pub1469338
Source
wos-lite
Published In
Medicine and Science in Sports and Exercise
Volume
52
Published Date
Start Page
302
End Page
302

Research Areas:

Abnormalities, Drug-Induced
Aldehydes
Benzopyrans
Calcium
Calibration
Cell Survival
DNA Replication
Dose-Response Relationship, Drug
Energy Metabolism
Fluorenes
Genotype
Half-Life
HeLa Cells
Heart
Heart Defects, Congenital
Humic Substances
Laboratories
Larva
Molecular Structure
Mutation
Neoplasm Proteins
Phosphorylation
Ponds
Proteolysis
Silver Nitrate
Solubility
Structure-Activity Relationship
Sulfides
Toxicity Tests
Transcriptome