Elizabeth J. Kopras

University of Cincinnati

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Co-Authors

Francis X. McCormack

University of Cincinnati Medical Center

Nishant Gupta

University of Cincinnati

Jane Yu

University of Auckland

Kathryn A. Wikenheiser‐Brokamp

Cincinnati Children's Hospital Medical Center

Yan Xu

Peking Union Medical College Hospital

Lori B. Pitstick

University of Cincinnati

Minzhe Guo

Cincinnati Children's Hospital Medical Center

Charles D. Ulrich

Kyushu University

Erik Y. Zhang

University of Cincinnati

Yasuaki Uehara

Sapporo Medical University

Cooperative Institutions

University of Cincinnati

144

University of Cincinnati Medical Center

117

Cincinnati Children's Hospital Medical Center

Sabin Vaccine Institute

Pulmonary Associates

Pulmonary and Critical Care Associates

Harvard University

University of Pennsylvania

Veterans Health Administration

Brigham and Women's Hospital

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PREDICTIVE MODELING OF TARGETED IMPROVEMENTS FOR COUNTY-LEVEL HPV VACCINE DELIVERY IN SOUTH CAROLINA

Annals of Epidemiology (2024)

Ashley A. White Renee Martin Brian Neelon Kathleen B. Cartmell Elizabeth Williams

South carolina

10.1016/j.annepidem.2024.07.025

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Citations (0)

Tuberin Regulates Prostaglandin Receptor–Mediated Viability, via Rheb, in mTORC1-Hyperactive Cells

Molecular Cancer Research (2017)

Chenggang Li Xiaolei Liu Liu Yang Erik Zhang K. Medepalli

Tuberous sclerosis complex (TSC) is a tumor-suppressor syndrome affecting multiple organs, including the brain, skin, kidneys, heart, and lungs. TSC is associated with mutations in TSC1 or TSC2, resulting in hyperactivation of mTOR complex 1 (mTORC1). Clinical trials demonstrate that mTORC1 inhibitors decrease tumor volume and stabilize lung function in TSC patients; however, mTOR inhibitors are cytostatic not cytocidal, and long-term benefits and toxicities are uncertain. Previously, we identified rapamycin-insensitive upregulation of cyclooxygenase 2 (PTGS2/COX2) and prostaglandin E2 (PGE2) production in TSC2-deficient cells and postulated that the action of excess PGE2 and its cognate receptors (EP) contributes to cell survival. In this study, we identify upregulation of EP3 (PTGER3) expression in TSC2-deficient cells, TSC renal angiomyolipomas, lymphangioleiomyomatosis lung nodules, and epileptic brain tubers. TSC2 negatively regulated EP3 expression via Rheb in a rapamycin-insensitive manner. The EP3 antagonist, L-798106, selectively suppressed the viability of TSC2-deficient cells in vitro and decreased the lung colonization of TSC2-deficient cells. Collectively, these data reveal a novel function of TSC2 and Rheb in the regulation of EP3 expression and cell viability.Implications: Therapeutic targeting of an aberrant PGE2-EP3 signaling axis may have therapeutic benefit for TSC patients and for other mTOR-hyperactive neoplasms. Mol Cancer Res; 15(10); 1318-30. ©2017 AACR.

RHEB

TSC2

TSC1

Lymphangioleiomyomatosis

Viability assay

10.1158/1541-7786.mcr-17-0077

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Citations (16)

Developing a Bidirectional Academic–Community Partnership with an Appalachian-American Community for Environmental Health Research and Risk Communication

Environmental Health Perspectives (2011)

Erin N. Haynes Caroline Beidler Richard Wittberg Lisa Melonçon Megan L. Parin

Marietta, Ohio, is an Appalachian-American community whose residents have long struggled with understanding their exposure to airborne manganese (Mn). Although community engagement in research is strongly endorsed by the National Institutes of Health and the National Institute of Environmental Health Sciences in particular, little has been documented demonstrating how an academic-community partnership that implements the community-based participatory research (CBPR) principles can be created and mobilized for research.We created a bidirectional, academic-community partnership with an Appalachian-American community to a) identify the community's thoughts and perceptions about local air quality, its effect on health, and the perception of risk communication sources and b) jointly develop and conduct environmental health research.We formed a community advisory board (CAB), jointly conducted pilot research studies, and used the results to develop a community-driven research agenda.Persons in the community were "very concerned" to "concerned" about local air quality (91%) and perceived the air quality to have a direct impact on their health and on their children's health (93% and 94%, respectively). The CAB identified the primary research question: "Does Mn affect the cognition and behavior of children?" Although the community members perceived research scientists as the most trusted and knowledgeable regarding risks from industrial emissions, they received very little risk information from research scientists.Engaging a community in environmental health research from its onset enhanced the quality and relevance of the research investigation. The CBPR principles were a useful framework in building a strong academic-community partnership. Because of the current disconnect between communities and research scientists, academic researchers should consider working collaboratively with community-based risk communication sources.

Community-Based Participatory Research

Community Engagement

Community Health

Community organization

10.1289/ehp.1003164

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Citations (45)

Single-cell multiomic analysis identifies a HOX-PBX gene network regulating the survival of lymphangioleiomyomatosis cells

Science Advances (2023)

Tasnim Olatoke Andrew Wagner Aristotelis Astrinidis Erik Y. Zhang Minzhe Guo

Lymphangioleiomyomatosis (LAM) is a rare, progressive lung disease that predominantly affects women. LAM cells carry

Lymphangioleiomyomatosis

TSC1

10.1126/sciadv.adf8549

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Citations (5)

RANKL Dependent Differentiation of Pulmonary Osteoclast-Like Cells in Silica-Induced Pulmonary Fibrosis

Yuka Hasegawa Yuya Tanaka Ciara M. Shaver Kevin K. Brown Charles Perkins

10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2253

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Citations (1)

MEK-1 plays an important role in EGF-induction and cAMP-mediated inhibition of ERK phosphorylation and G1åS phase transition in ductal pancreatic cancer cells

Gastroenterology (1998)

Elizabeth J. Kopras James Cornelius George F. Babcock Charles D. Ulrich

10.1016/s0016-5085(98)82567-5

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Citations (3)

Alpha-1 Antitrypsin Limits Neutrophil Extracellular Trap Disruption of Airway Epithelial Barrier Function

bioRxiv (Cold Spring Harbor Laboratory) (2022)

KM Hudock MS Collins M. Imbrogno EL Kramer John J. Brewington

Abstract Neutrophil extracellular traps contribute to lung injury in cystic fibrosis and asthma, but the mechanisms are poorly understood. We sought to understand the impact of human NETs on barrier function in primary human bronchial epithelial and a human airway epithelial cell line. We demonstrate that NETs disrupt airway epithelial barrier function by decreasing transepithelial electrical resistance and increasing paracellular flux, partially by NET-induced airway cell apoptosis. NETs selectively impact the expression of tight junction genes claudins 4, 8 and 11. Bronchial epithelia exposed to NETs demonstrate visible gaps in E-cadherin staining, a decrease in full-length E-cadherin protein and the appearance of cleaved E-cadherin peptides. Pretreatment of NETs with alpha-1 antitrypsin (A1AT) inhibits NET serine protease activity, limits E-cadherin cleavage, decreases bronchial cell apoptosis and preserves epithelial integrity. In conclusion, NETs disrupt human airway epithelial barrier function through bronchial cell death and degradation of E-cadherin, which are limited by exogenous A1AT.

Barrier function

Neutrophil Extracellular Traps

Neutrophil elastase

Paracellular transport

10.1101/2022.03.18.484920

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Citations (3)

Hereditary pancreatitis: Epidemiology, molecules, mutations, and models

Journal of Laboratory and Clinical Medicine (2000)

Charles D. Ulrich Elizabeth J. Kopras Ying Wu Susan A. Ward

Hereditary pancreatitis

Pathogenesis

10.1067/mlc.2000.109405

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Citations (11)

Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease

Endocrine Related Cancer (2013)

Elizabeth J. Kopras Veena Potluri Mei-Ling Bermúdez Karin Williams Scott M. Belcher

Development and fate of the stem cell are regulated by extrinsic signals from the environment. Endocrine-disrupting chemicals which perturb hormonal signaling in utero and during early childhood may cause deregulation of multiple developmental processes, ranging from breakdown of stem cell niche architecture, developmental reprograming and altered stem cell fate to impaired organ and gonad development and sexual differentiation. Therefore, study of the environmental effects on stem cell integrity and normal development is a new and emerging focus for developmental biologists and cell toxicologists. When combined with new human and mouse stem cell-based models, stem cell differentiation dynamics can be studied in more biologically relevant ways. In this study, we review the current status of our understanding of the molecular mechanisms by which endocrine disruptors alter embryonic stem cell and adult stem/progenitor cell fate, organ development, cancer stem cell activity, and tumorigenesis.

Cell fate determination

Progenitor

10.1530/erc-13-0360

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Citations (34)

Menstrual Cycle-Related Symptom Variability in Patients with Lymphangioleiomyomatosis

Brian M. Shaw Elizabeth J. Kopras Nishant Gupta

Lymphangioleiomyomatosis

10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1412

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Citations (1)