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Duan, Q

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Duan

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Duan, Q
Author's Publications: search.filters.isAuthorOfPublication.192b1669-ca26-48eb-b5ee-a5f55165c405

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    RNA-Seq Transcriptome Profiling Identifies CRISPLD2 as a Glucocorticoid Responsive Gene that Modulates Cytokine Function in Airway Smooth Muscle Cells
    (Public Library of Science, 2014) Himes, Blanca; Jiang, Xiaofeng; Wagner, Peter; Hu, Ruoxi; Wang, Qiyu; Klanderman, Barbara; Whitaker, Reid M.; Duan, Q; Lasky-Su, Jessica; Nikolos, Christina; Jester, William; Johnson, Martin; Panettieri, Reynold A.; Tantisira, Kelan; Weiss, Scott; Lu, Quan
    Asthma is a chronic inflammatory respiratory disease that affects over 300 million people worldwide. Glucocorticoids are a mainstay therapy for asthma because they exert anti-inflammatory effects in multiple lung tissues, including the airway smooth muscle (ASM). However, the mechanism by which glucocorticoids suppress inflammation in ASM remains poorly understood. Using RNA-Seq, a high-throughput sequencing method, we characterized transcriptomic changes in four primary human ASM cell lines that were treated with dexamethasone—a potent synthetic glucocorticoid (1 µM for 18 hours). Based on a Benjamini-Hochberg corrected p-value <0.05, we identified 316 differentially expressed genes, including both well known (DUSP1, KLF15, PER1, TSC22D3) and less investigated (C7, CCDC69, CRISPLD2) glucocorticoid-responsive genes. CRISPLD2, which encodes a secreted protein previously implicated in lung development and endotoxin regulation, was found to have SNPs that were moderately associated with inhaled corticosteroid resistance and bronchodilator response among asthma patients in two previously conducted genome-wide association studies. Quantitative RT-PCR and Western blotting showed that dexamethasone treatment significantly increased CRISPLD2 mRNA and protein expression in ASM cells. CRISPLD2 expression was also induced by the inflammatory cytokine IL1β, and small interfering RNA-mediated knockdown of CRISPLD2 further increased IL1β-induced expression of IL6 and IL8. Our findings offer a comprehensive view of the effect of a glucocorticoid on the ASM transcriptome and identify CRISPLD2 as an asthma pharmacogenetics candidate gene that regulates anti-inflammatory effects of glucocorticoids in the ASM.
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    A DNA methylation biomarker of alcohol consumption
    (Springer Nature, 2016) Liu, C; Marioni, R E; Hedman, Å K; Pfeiffer, L; Tsai, P-C; Reynolds, L M; Just, A C; Duan, Q; Boer, C G; Tanaka, T; Elks, C E; Aslibekyan, S; Brody, J A; Kühnel, B; Herder, C; Almli, L M; Zhi, D; Wang, Y; Huan, T; Yao, C; Mendelson, M M; Joehanes, Roby; Liang, Liming; Love, S-A; Guan, W; Shah, S; McRae, A F; Kretschmer, A; Prokisch, H; Strauch, K; Peters, A; Visscher, P M; Wray, N R; Guo, X; Wiggins, K L; Smith, A K; Binder, E B; Ressler, Kerry; Irvin, M R; Absher, D M; Hernandez, D; Ferrucci, L; Bandinelli, S; Lohman, K; Ding, J; Trevisi, Letizia; Gustafsson, S; Sandling, J H; Stolk, L; Uitterlinden, A G; Yet, I; Castillo-Fernandez, J E; Spector, T D; Schwartz, Joel; Vokonas, P; Lind, L; Li, Y; Fornage, M; Arnett, D K; Wareham, N J; Sotoodehnia, N; Ong, K K; van Meurs, J B J; Conneely, K N; Baccarelli, A A; Deary, I J; Bell, J T; North, K E; Liu, Y; Waldenberger, M; London, S J; Ingelsson, E; Levy, D
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    Publication
    A genome-wide association study of bronchodilator response in asthmatics
    (Nature Publishing Group, 2013) Duan, Q; Lasky-Su, Jessica; Himes, Blanca; Qiu, Weiliang; Litonjua, Augusto A.; Damask, Amy; Lazarus, Richard; Klanderman, Barbara; Irvin, Charles G.; Peters, Stephen P; Hanrahan, John P; Lima, John J.; Martinez, Fernando D.; Mauger, David; Chinchilli, Vernon M.; Soto-Quiros, Manuel; Avila, Lydiana; Celedón, Juan C.; Lange, Christoph; Weiss, Scott; Tantisira, Kelan
    Reversibility of airway obstruction in response to β2-agonists is highly variable among asthmatics, which is partially attributed to genetic factors. In a genome-wide association study of acute bronchodilator response (BDR) to inhaled albuterol, 534,290 single nucleotide polymorphisms (SNPs) were tested in 403 white trios from the Childhood Asthma Management Program using five statistical models to determine the most robust genetic associations. The primary replication phase included 1397 polymorphisms in three asthma trials (pooled n=764). The second replication phase tested 13 SNPs in three additional asthma populations (n=241, n=215, and n=592). An intergenic SNP on chromosome 10, rs11252394, proximal to several excellent biological candidates, significantly replicated (p=1.98×10−7) in the primary replication trials. An intronic SNP (rs6988229) in the collagen (COL22A1) locus also provided strong replication signals (p=8.51×10−6). This study applied a robust approach for testing the genetic basis of BDR and identified novel loci associated with this drug response in asthmatics.