Elizabeth Alison Thompson

Works (7)

Updated: August 6th, 2023 21:15

2018 journal article

Role of p53 in the chronic pulmonary immune response to tangled or rod-like multi-walled carbon nanotubes

NANOTOXICOLOGY, 12(9), 975–991.

By: K. Duke n, E. Thompson n, M. Ihrie n, A. Taylor-Just n, E. Ash n, K. Shipkowski n, J. Hall n , D. Tokarz n ...

author keywords: Caron nanotubes; immunotoxicology; cancer; granuloma; p53
MeSH headings : Animals; Dose-Response Relationship, Drug; Granuloma, Respiratory Tract / chemically induced; Granuloma, Respiratory Tract / genetics; Granuloma, Respiratory Tract / immunology; Inhalation Exposure; Lung / drug effects; Lung / immunology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Nanotubes, Carbon / chemistry; Nanotubes, Carbon / toxicity; Surface Properties; Tertiary Lymphoid Structures / chemically induced; Tertiary Lymphoid Structures / genetics; Tertiary Lymphoid Structures / immunology; Tumor Suppressor Protein p53 / genetics; Tumor Suppressor Protein p53 / physiology
TL;DR: Findings indicate that a combination of p53 deficiency and physicochemical characteristics including nanotube geometry are factors in susceptibility to MWCNT-induced lymphoid infiltration and granuloma formation. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Sources: Web Of Science, NC State University Libraries
Added: March 4, 2019

2017 journal article

STAT1-dependent and -independent pulmonary allergic and fibrogenic responses in mice after exposure to tangled versus rod-like multi-walled carbon nanotubes

PARTICLE AND FIBRE TOXICOLOGY, 14.

By: K. Duke n, A. Taylor-Just n, M. Ihrie n, K. Shipkowski n, E. Thompson n, E. Dandley n, G. Parsons n , J. Bonner n 

author keywords: Carbon nanotubes; Lung; Fibrosis; Growth factors; Transcription factors
MeSH headings : Animals; Bronchoalveolar Lavage Fluid / chemistry; Cell Proliferation / drug effects; Cytokines / metabolism; Epithelial Cells / drug effects; Epithelial Cells / metabolism; Epithelial Cells / pathology; Genetic Predisposition to Disease; Granuloma, Respiratory Tract / chemically induced; Granuloma, Respiratory Tract / metabolism; Granuloma, Respiratory Tract / pathology; Immunoglobulin E / blood; Lung / drug effects; Lung / metabolism; Lung / pathology; Male; Mice, Knockout; Nanotubes, Carbon / chemistry; Nanotubes, Carbon / toxicity; Phenotype; Phosphorylation; Pneumonia / chemically induced; Pneumonia / metabolism; Pneumonia / pathology; Pulmonary Fibrosis / chemically induced; Pulmonary Fibrosis / genetics; Pulmonary Fibrosis / metabolism; Pulmonary Fibrosis / pathology; Respiratory Hypersensitivity / chemically induced; Respiratory Hypersensitivity / genetics; Respiratory Hypersensitivity / metabolism; Respiratory Hypersensitivity / pathology; Risk Assessment; STAT1 Transcription Factor / deficiency; STAT1 Transcription Factor / genetics; STAT1 Transcription Factor / metabolism; Signal Transduction / drug effects; Smad2 Protein / metabolism; Smad3 Protein / metabolism; Time Factors; Transforming Growth Factor beta1 / metabolism
TL;DR: Rigidity plays a key role in the toxicity of MWCNTs and results in increased inflammatory, immunologic, and fibrogenic effects in the lung, and both rigidity and genetic susceptibility should be major considerations for risk assessment of MMWNTs. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Sources: Web Of Science, NC State University Libraries
Added: August 6, 2018

2015 journal article

Role of Signal Transducer and Activator of Transcription 1 in Murine Allergen-Induced Airway Remodeling and Exacerbation by Carbon Nanotubes

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 53(5), 625–636.

By: E. Thompson n, B. Sayers n, E. Glista-Baker n, K. Shipkowski n, M. Ihrie n, K. Duke n, A. Taylor n, J. Bonner n 

author keywords: asthma; allergen; nanomaterials; carbon nanotubes; airway remodeling
MeSH headings : Allergens / pharmacology; Animals; Bronchoalveolar Lavage Fluid / chemistry; Eosinophils / drug effects; Eosinophils / immunology; Eosinophils / pathology; Epithelial Cells / drug effects; Epithelial Cells / immunology; Epithelial Cells / pathology; Gene Expression Regulation; Goblet Cells / drug effects; Goblet Cells / immunology; Goblet Cells / pathology; Interleukin-10 / genetics; Interleukin-10 / immunology; Interleukin-13 / genetics; Interleukin-13 / immunology; Male; Mice; Mice, Knockout; Nanotubes / adverse effects; Neutrophils / drug effects; Neutrophils / immunology; Neutrophils / pathology; Osteopontin / genetics; Osteopontin / immunology; Ovalbumin / immunology; Respiratory Hypersensitivity / etiology; Respiratory Hypersensitivity / genetics; Respiratory Hypersensitivity / immunology; Respiratory Hypersensitivity / pathology; STAT1 Transcription Factor / deficiency; STAT1 Transcription Factor / genetics; STAT1 Transcription Factor / immunology; Signal Transduction; T-Lymphocytes, Helper-Inducer / drug effects; T-Lymphocytes, Helper-Inducer / immunology; T-Lymphocytes, Helper-Inducer / pathology; Transforming Growth Factor beta1 / genetics; Transforming Growth Factor beta1 / immunology; Transforming Growth Factor beta1 / pharmacology; Tumor Necrosis Factor-alpha / genetics; Tumor Necrosis Factor-alpha / immunology
TL;DR: A protective role for STAT1 is supported in chronic AAI and exacerbation of remodeling caused by MWCNTs and fibroblasts isolated from the lungs of Stat1(-/-) mice produced significantly more collagen mRNA and protein in response to transforming growth factor-β1 compared with WT lung fibro Blasts. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Sources: Web Of Science, NC State University Libraries
Added: August 6, 2018

2014 journal article

Atomic Layer Deposition Coating of Carbon Nanotubes with Aluminum Oxide Alters Pro-Fibrogenic Cytokine Expression by Human Mononuclear Phagocytes In Vitro and Reduces Lung Fibrosis in Mice In Vivo

PLOS ONE, 9(9).

By: A. Taylor n, C. McClure n, K. Shipkowski n, E. Thompson n, S. Hussain *, S. Garantziotis *, G. Parsons n , J. Bonner n 

Contributors: A. Taylor n, C. McClure n, K. Shipkowski n, E. Thompson n, S. Hussain *, S. Garantziotis *, G. Parsons n , J. Bonner n 

MeSH headings : Aluminum Oxide / pharmacology; Animals; Cell Death / drug effects; Cell Line; Cytokines / metabolism; Humans; Inflammation / pathology; Interleukin-1beta / biosynthesis; Interleukin-6 / metabolism; Leukocytes, Mononuclear / drug effects; Leukocytes, Mononuclear / metabolism; Lung / drug effects; Lung / metabolism; Lung / pathology; Macrophages / drug effects; Macrophages / metabolism; Macrophages / ultrastructure; Mice, Inbred C57BL; Nanotechnology / methods; Nanotubes, Carbon / chemistry; Nanotubes, Carbon / ultrastructure; Osteopontin / metabolism; Phagocytes / drug effects; Phagocytes / metabolism; Pulmonary Fibrosis; Soot / pharmacology; Surface Properties; Tumor Necrosis Factor-alpha / metabolism
TL;DR: Findings indicate that ALD thin film coating of MWCNTs with Al2O3 reduces fibrosis in mice and that in vitro phagocyte expression of IL-6, TNF-α, and OPN, but not IL-1β, predict M WCNT-induced fibrosisIn the lungs of mice in vivo. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Sources: Web Of Science, ORCID, NC State University Libraries
Added: August 6, 2018

2012 journal article

Nickel Nanoparticles Enhance Platelet-Derived Growth Factor-Induced Chemokine Expression by Mesothelial Cells via Prolonged Mitogen-Activated Protein Kinase Activation

AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 47(4), 552–561.

By: E. Glista-Baker n, A. Taylor n, B. Sayers n, E. Thompson n & J. Bonner n 

author keywords: nanoparticles; metals; lung; pleura; chemokines
MeSH headings : Acetylcysteine / pharmacology; Analysis of Variance; Animals; Antioxidants / pharmacology; Cell Line; Chemokine CCL2 / genetics; Chemokine CCL2 / metabolism; Chemokine CXCL10 / genetics; Chemokine CXCL10 / metabolism; Enzyme Activation; Epithelial Cells / drug effects; Epithelial Cells / enzymology; Epithelial Cells / ultrastructure; Gene Expression / drug effects; Gene Expression Regulation / drug effects; Hypoxia-Inducible Factor 1, alpha Subunit / genetics; Hypoxia-Inducible Factor 1, alpha Subunit / metabolism; MAP Kinase Signaling System; Metal Nanoparticles; Mitogen-Activated Protein Kinases / metabolism; Nickel / metabolism; Nickel / pharmacology; Phosphorylation; Platelet-Derived Growth Factor / physiology; Pleura / cytology; Protein Processing, Post-Translational; Rats; Receptors, Platelet-Derived Growth Factor / metabolism
TL;DR: It is found that NiNPs enhance the activity of PDGF in regulating chemokine production in NRM2 cells through a mechanism involving reactive oxygen species generation and prolonged activation of ERK-1,2. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Sources: Web Of Science, NC State University Libraries
Added: August 6, 2018

2011 journal article

C/EBP alpha Expression Is Downregulated in Human Nonmelanoma Skin Cancers and Inactivation of C/EBP alpha Confers Susceptibility to UVB-Induced Skin Squamous Cell Carcinomas

JOURNAL OF INVESTIGATIVE DERMATOLOGY, 131(6), 1339–1346.

By: E. Thompson n, S. Zhu n, J. Hall n , J. House n , R. Ranjan n, J. Burr n, Y. He *, D. Owens *, R. Smart n 

Contributors: E. Thompson n, S. Zhu n, J. Hall n , J. House n , R. Ranjan n, J. Burr n, Y. He *, D. Owens *, R. Smart n 

MeSH headings : Animals; CCAAT-Enhancer-Binding Protein-alpha / analysis; CCAAT-Enhancer-Binding Protein-alpha / physiology; Carcinoma, Squamous Cell / chemistry; Carcinoma, Squamous Cell / etiology; Cell Cycle; Cells, Cultured; Genes, p53; Humans; Keratosis, Actinic / metabolism; Male; Mice; Mice, Hairless; Mice, Inbred C57BL; Mutation; Neoplasms, Radiation-Induced / etiology; Precancerous Conditions / chemistry; Skin / metabolism; Skin / radiation effects; Skin Neoplasms / chemistry; Skin Neoplasms / etiology; Ultraviolet Rays / adverse effects
TL;DR: It is observed that C/EBPα is induced in normal human epidermal keratinocytes and in the epidermis of human subjects exposed to UVB radiation, and loss of C/ EBPα confers susceptibility toUVB-induced skin SCCs involving defective cell cycle arrest in response to UVBs. (via Semantic Scholar)
UN Sustainable Development Goal Categories
3. Good Health and Well-being (Web of Science; OpenAlex)
Sources: Web Of Science, NC State University Libraries, ORCID
Added: August 6, 2018

2009 journal article

C/EBP alpha expression is partially regulated by C/EBP beta in response to DNA damage and C/EBP alpha-deficient fibroblasts display an impaired G(1) checkpoint

ONCOGENE, 28(36), 3235–3245.

By: R. Ranjan n, E. Thompson n, K. Yoon* & R. Smart n 

author keywords: C/EBP; DNA damage response; G(1)/S transition; p53
MeSH headings : Animals; Blotting, Western; CCAAT-Enhancer-Binding Protein-alpha / genetics; CCAAT-Enhancer-Binding Protein-alpha / metabolism; CCAAT-Enhancer-Binding Protein-beta / genetics; CCAAT-Enhancer-Binding Protein-beta / metabolism; DNA Damage; Female; Fibroblasts / drug effects; Fibroblasts / metabolism; Fibroblasts / radiation effects; Flow Cytometry; G1 Phase; Gene Expression; Male; Methylnitronitrosoguanidine / toxicity; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Mice, Knockout; Reverse Transcriptase Polymerase Chain Reaction; S Phase; Time Factors; Ultraviolet Rays
TL;DR: This study shows a novel function for C/EBPβ in the regulation of C/N′-nitro-N-nitrosoguanidine-treated fibroblasts and provides definitive genetic evidence that C-EBPα has a critical role in the DNA damage G1 checkpoint. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Sources: Web Of Science, NC State University Libraries
Added: August 6, 2018

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