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1. IL-1/inhibitory κB kinase ε–induced glycolysis augment epithelial effector function and promote allergic airways disease

Author

Qian, Xi, Aboushousha, Reem, van de Wetering, Cheryl, Chia, Shi B., Amiel, Eyal, Schneider, Robert W., van der Velden, Jos L.J., Lahue, Karolyn G., Hoagland, Daisy A., Casey, Dylan T., Daphtary, Nirav, Ather, Jennifer L., Randall, Matthew J., Aliyeva, Minara, Black, Kendall E., Chapman, David G., Lundblad, Lennart K.A., McMillan, David H., Dixon, Anne E., Anathy, Vikas, Irvin, Charles G., Poynter, Matthew E., Wouters, Emiel F.M., Vacek, Pamela M., Henket, Monique, Schleich, Florence, Louis, Renaud, van der Vliet, Albert, and Janssen-Heininger, Yvonne M.W.

Published
2018
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2. Data from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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3. Data from Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, primary, Kozul, Courtney D., primary, Black, Kendall E., primary, Singh, Samer, primary, Gosse, Julie A., primary, DiRenzo, James, primary, Martin, Kathleen A., primary, Wang, Baolin, primary, Hamilton, Joshua W., primary, Karagas, Margaret R., primary, and Robbins, David J., primary

Published
2023
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4. Supplementary Table 1 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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5. Supplementary Figure 1 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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6. Supplementary Figure 2 from Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, primary, Kozul, Courtney D., primary, Black, Kendall E., primary, Singh, Samer, primary, Gosse, Julie A., primary, DiRenzo, James, primary, Martin, Kathleen A., primary, Wang, Baolin, primary, Hamilton, Joshua W., primary, Karagas, Margaret R., primary, and Robbins, David J., primary

Published
2023
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7. Supplementary Figure 4 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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8. Supplementary Figure 5 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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9. Supplementary Table 2 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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10. Supplementary Figure 3 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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11. Supplementary Figure 6 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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12. Supplementary Table Legends 1-2, Figure Legends 1-6 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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13. Supplementary Figure 1 A-B from Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, primary, Kozul, Courtney D., primary, Black, Kendall E., primary, Singh, Samer, primary, Gosse, Julie A., primary, DiRenzo, James, primary, Martin, Kathleen A., primary, Wang, Baolin, primary, Hamilton, Joshua W., primary, Karagas, Margaret R., primary, and Robbins, David J., primary

Published
2023
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14. Supplementary Figure 2 from Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, primary, Liang Fei, Dennis, primary, Black, Kendall E., primary, Goetz, John A., primary, Tokhunts, Robert, primary, Giambelli, Camilla, primary, Rodriguez-Blanco, Jezabel, primary, Long, Jun, primary, Lee, Ethan, primary, Briegel, Karoline J., primary, Bejarano, Pablo A., primary, Dmitrovsky, Ethan, primary, Capobianco, Anthony J., primary, and Robbins, David J., primary

Published
2023
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15. Supplementary Figure 1C from Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, primary, Kozul, Courtney D., primary, Black, Kendall E., primary, Singh, Samer, primary, Gosse, Julie A., primary, DiRenzo, James, primary, Martin, Kathleen A., primary, Wang, Baolin, primary, Hamilton, Joshua W., primary, Karagas, Margaret R., primary, and Robbins, David J., primary

Published
2023
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16. Supplementary Table 1 from Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, primary, Kozul, Courtney D., primary, Black, Kendall E., primary, Singh, Samer, primary, Gosse, Julie A., primary, DiRenzo, James, primary, Martin, Kathleen A., primary, Wang, Baolin, primary, Hamilton, Joshua W., primary, Karagas, Margaret R., primary, and Robbins, David J., primary

Published
2023
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17. Supplementary Figure 4 from Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, primary, Kozul, Courtney D., primary, Black, Kendall E., primary, Singh, Samer, primary, Gosse, Julie A., primary, DiRenzo, James, primary, Martin, Kathleen A., primary, Wang, Baolin, primary, Hamilton, Joshua W., primary, Karagas, Margaret R., primary, and Robbins, David J., primary

Published
2023
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18. Supplementary Materials, Figure Legends 1-4 from Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, primary, Kozul, Courtney D., primary, Black, Kendall E., primary, Singh, Samer, primary, Gosse, Julie A., primary, DiRenzo, James, primary, Martin, Kathleen A., primary, Wang, Baolin, primary, Hamilton, Joshua W., primary, Karagas, Margaret R., primary, and Robbins, David J., primary

Published
2023
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24. Epithelial Nuclear Factor- kappa B orchestrates house dust mite-induced airway inflammation, hyperresponsiveness, and fibrotic remodeling

Author

Tully, Jane E., Hoffman, Sidra M., Lahue, Karolyn G., Nolin, James D., Anathy, Vikas, Lundblad, Lennart K. A., Daphtary, Nirav, Aliyeva, Minara, Black, Kendall E., Dixon, Anne E., Poynter, Matthew E., Irvin, Charles G., and Janssen-Heininger, Yvonne M. W.

Subjects
Neutrophils, Mice, Transgenic, Article, Epithelium, Cell Line, Mice, NF-KappaB Inhibitor alpha, Animals, Humans, Uteroglobin, Single-Blind Method, Antigens, Dermatophagoides, Lymphocytes, RNA, Messenger, Bronchioles, Lung, Administration, Intranasal, Metaplasia, Mice, Inbred BALB C, Interleukin-13, Macrophages, Pyroglyphidae, NF-kappa B, Epithelial Cells, respiratory system, Fibrosis, respiratory tract diseases, Eosinophils, Gene Expression Regulation, Airway Remodeling, I-kappa B Proteins, Inflammation Mediators, Bronchoalveolar Lavage Fluid
Abstract

NF-κB activation within the epithelium has been implicated in the pathogenesis of asthma, yet the exact role of epithelial NF-κB in allergen-induced inflammation and airway remodeling remains unclear. In the present study, we utilized an intranasal House Dust Mite (HDM) extract exposure regimen time course in BALB/c mice to evaluate inflammation, NF-κB activation, airway hyperresponsiveness (AHR), and airway remodeling. We utilized CC10-IκBαSR transgenic mice to evaluate the functional importance of epithelial NF-κB in response to HDM. After a single exposure of HDM, mRNA expression of pro-inflammatory mediators was significantly elevated in lung tissue of WT mice, in association with increases in nuclear RelA and RelB, components of the classical and alternative NF-κB pathway, respectively, in the bronchiolar epithelium. In contrast, CC10-IκBαSR mice displayed marked decreases in nuclear RelA and RelB and mRNA expression of pro-inflammatory mediators compared to WT mice. After 15 challenges with HDM, WT mice exhibited increases in inflammation, airway hyperresponsiveness, mucus metaplasia and peri-bronchiolar fibrosis. CC10-IκBαSR transgenic mice displayed marked decreases in neutrophilic infiltration, tissue damping, and elastance parameters, in association will less peri-bronchiolar fibrosis and decreases in nuclear RelB in lung tissue. However, central airway resistance and mucus metaplasia remained elevated in CC10-IκBαSR transgenic mice, in association with continued presence of lymphocytes, and partial decreases in eosinophils and IL-13. The current study demonstrates that following airway exposure with an asthma-relevant allergen, activation of classical and alternative NF-κB pathways occur within the airway epithelium and may coordinately contribute to allergic inflammation, AHR and fibrotic airway remodeling.

Published
2013

26. Epithelial NF-κB Orchestrates House Dust Mite–Induced Airway Inflammation, Hyperresponsiveness, and Fibrotic Remodeling

Author

Tully, Jane E., primary, Hoffman, Sidra M., additional, Lahue, Karolyn G., additional, Nolin, James D., additional, Anathy, Vikas, additional, Lundblad, Lennart K. A., additional, Daphtary, Nirav, additional, Aliyeva, Minara, additional, Black, Kendall E., additional, Dixon, Anne E., additional, Poynter, Matthew E., additional, Irvin, Charles G., additional, and Janssen-Heininger, Yvonne M. W., additional

Published
2013
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27. Obesity and Asthma

Author

Sideleva, Olga, primary, Suratt, Benjamin T., additional, Black, Kendall E., additional, Tharp, William G., additional, Pratley, Richard E., additional, Forgione, Patrick, additional, Dienz, Oliver, additional, Irvin, Charles G., additional, and Dixon, Anne E., additional

Published
2012
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30. Hedgehog-Producing Cancer Cells Respond to and Require Autocrine Hedgehog Activity

Author

Singh, Samer, primary, Wang, Zhiqiang, additional, Liang Fei, Dennis, additional, Black, Kendall E., additional, Goetz, John A., additional, Tokhunts, Robert, additional, Giambelli, Camilla, additional, Rodriguez-Blanco, Jezabel, additional, Long, Jun, additional, Lee, Ethan, additional, Briegel, Karoline J., additional, Bejarano, Pablo A., additional, Dmitrovsky, Ethan, additional, Capobianco, Anthony J., additional, and Robbins, David J., additional

Published
2011
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31. Activation of Hedgehog Signaling by the Environmental Toxicant Arsenic May Contribute to the Etiology of Arsenic-Induced Tumors

Author

Fei, Dennis Liang, primary, Li, Hua, additional, Kozul, Courtney D., additional, Black, Kendall E., additional, Singh, Samer, additional, Gosse, Julie A., additional, DiRenzo, James, additional, Martin, Kathleen A., additional, Wang, Baolin, additional, Hamilton, Joshua W., additional, Karagas, Margaret R., additional, and Robbins, David J., additional

Published
2010
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33. Epithelial NF-kB Orchestrates House Dust Mite-Induced Airway Inflammation, Hyperresponsiveness, and Fibrotic Remodeling.

Author

Tully, Jane E., Hoffman, Sidra M., Lahue, Karolyn G., Nolin, James D., Anathy, Vikas, Lundblad, Lennart K. A., Daphtary, Nirav, Aliyeva, Minara, Black, Kendall E., Dixon, Anne E., Poynter, Matthew E., Irvin, Charles G., and Janssen-Heininger, Yvonne M. W.

Subjects
*RESPIRATORY obstructions, *GENETICS of asthma, *INTRANASAL medication, *RESPIRATORY therapy, *EPITHELIAL cells, *HOUSE dust mites, *TRANSGENIC mice
Abstract

NF-kB activation within the epithelium has been implicated in the pathogenesis of asthma, yet the exact role of epithelial NF-kB in allergen-induced inflammation and airway remodeling remains unclear. In the current study, we used an intranasal house dust mite (HDM) extract exposure regimen time course in BALB/c mice to evaluate inflammation, NF-kB activation, airway hyperresponsiveness (AHR), and airway remodeling. We used CC10-IkBaSR transgenic mice to evaluate the functional importance of epithelial NF-kB in response to HDM. After a single exposure of HDM, mRNA expression of proinflammatory mediators was significantly elevated in lung tissue of wild-type (WT) mice, in association with increases in nuclear RelA and RelB, components of the classical and alternative NF-kB pathway, respectively, in the bronchiolar epithelium. In contrast, CC10-IkBaSR mice displayed marked decreases in nuclear RelA and RelB and mRNA expression of proinflammatory mediators compared with WT mice. After 15 challenges with HDM, WT mice exhibited increases in inflammation, AHR, mucus metaplasia, and peribronchiolar fibrosis. CC10-IkBaSR transgenic mice displayed marked decreases in neutrophilic infiltration, tissue damping, and elastance parameters, in association will less peribronchiolar fibrosis and decreases in nuclear RelB in lung tissue. However, central airway resistance and mucus metaplasia remained elevated in CC10-IkBaSR transgenic mice, in association with the continued presence of lymphocytes, and partial decreases in eosinophils and IL-13. The current study demonstrates that following airway exposure with an asthma-relevant allergen, activation of classical and alternative NF-kB pathways occurs within the airway epithelium and may coordinately contribute to allergic inflammation, AHR, and fibrotic airway remodeling. [ABSTRACT FROM AUTHOR]

Published
2013
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