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15 results on '"Qin, Liya"'

6. Neuroimmune function and the consequences of alcohol exposure

Author

Crews, Fulton T., Sarkar, Dipak K., Qin, Liya, Zou, Jian, Boyadjieva, Nadka, and Vetreno, Ryan P.

Subjects
Neurons, Methyl aspartate, Drinking of alcoholic beverages, Genes, Glutamate, Aspartate, B cells, Alcohols, Anopheles, Neurophysiology, Health
Abstract

Induction of neuroimmune genes by binge drinking increases neuronal excitability and oxidative stress, contributing to the neurobiotogy of alcohol dependence and causing neurodegeneration. Ethanol exposure activates signaling pathways featuring high-mobility [...]

Published
2015

7. NADPH oxidase and endoplasmic reticulum stress is associated with neuronal degeneration in orbitofrontal cortex of individuals with alcohol use disorder.

Author

Qin, Liya, Vetreno, Ryan P., and Crews, Fulton T.

Subjects
*ALCOHOLISM, *PREFRONTAL cortex, *ENDOPLASMIC reticulum, *NADPH oxidase, *GLUCOSE-regulated proteins, *PROTEIN kinases, *TRANSCRIPTION factors
Abstract

Many disorders of the central nervous system (CNS), including alcohol use disorder (AUD), are associated with induction of proinflammatory neuroimmune signalling and neurodegeneration. In previous studies, we found increased expression of Toll‐like receptors (TLRs), activated NF‐κB p65 (RELA), and other proinflammatory signalling molecules. Proinflammatory NADPH oxidases generate reactive oxygen species, which are linked to neurodegeneration. We tested the hypothesis that AUD increased RELA activation increases NADPH oxidase‐oxidative stress and endoplasmic reticulum (ER) stress cell death cascades in association with neuronal cell death in the human orbitofrontal cortex (OFC). In the AUD OFC, we report mRNA induction of several NADPH oxidases, the dual oxidase DUOX2, and the oxidative stress lipid peroxidation marker 4‐HNE and the DNA oxidation marker 8‐OHdG that correlate with RELA, a marker of proinflammatory NF‐κB activation. This was accompanied by increased expression of the ER stress‐associated regulator protein glucose‐regulated protein 78 (GRP78), transmembrane sensors activating transcription factor 6 (ATF6), protein kinase RNA‐like endoplasmic reticulum kinase (PERK), and inositol‐requiring kinase/endonuclease 1 (pIRE1), and the pro‐apoptotic transcription factor C/EBP homologous protein (CHOP). Expression of NADPH oxidase‐oxidative stress markers correlate with ER stress‐associated molecules. Induction of oxidative stress and ER stress signalling pathways correlate with expression of cell death‐associated caspases and neuronal cell loss. These data support the hypothesis that proinflammatory RELA‐mediated induction of NADPH oxidase‐oxidative stress and ER stress‐associated signalling cascades is associated with neuronal cell death in the post‐mortem human OFC of individuals with AUD. [ABSTRACT FROM AUTHOR]

Published
2023
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10. Preparation of docetaxel‑loaded, glycyrrhetinic acid‑modified nanoparticles and their liver‑targeting and antitumor activity

Author

Xue, Hantao, primary, Qin, Liya, additional, Zhang, Longxiang, additional, Li, Xiaocheng, additional, Wu, Fei, additional, Wang, Weiyu, additional, Wang, Chen, additional, Diao, Wenbin, additional, Jiang, Bin, additional, Lian, Bo, additional, Wu, Jingliang, additional, Bai, Jingkun, additional, Sun, Tongyi, additional, Zhao, Chunling, additional, Qu, Meihua, additional, Yu, Wenjing, additional, Wang, Yubing, additional, and Gao, Zhiqin, additional

Published
2021
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12. The Cortical Neuroimmune Regulator TANK Affects Emotional Processing and Enhances Alcohol Drinking: A Translational Study

Author

Müller, Christian P., Chu, Congying, Qin, Liya, Liu, Chunyu, Xu, Bing, Gao, He, Ruggeri, Barbara, Hieber, Saskia, Schneider, Julia, Jia, Tianye, Tay, Nicole, Akira, Shizuo, Satoh, Takashi, Banaschewski, Tobias, Bokde, Arun L. W., Bromberg, Uli, Büchel, Christian, Quinlan, Erin Burke, Flor, Herta, Frouin, Vincent, Garavan, Hugh, Gowland, Penny, Heinz, Andreas, Ittermann, Bernd, Martinot, Jean-Luc, Martinot, Marie-Laure Paillère, Artiges, Eric, Lemaitre, Herve, Nees, Frauke, Papadopoulos Orfanos, Dimitri, Paus, Tomáš, Poustka, Luise, Millenet, Sabina, Fröhner, Juliane H., Smolka, Michael N., Walter, Henrik, Whelan, Robert, Bakalkin, Georgy, Liu, Yun, Desrivières, Sylvane, Elliott, Paul, Eulenburg, Volker, Levy, Daniel, Crews, Fulton, Schumann, Gunter, and Medical Research Council (MRC)

Subjects
Male, Mice, 129 Strain, Adolescent, Alcohol Drinking, Neuroimmunomodulation, Emotions, drinking, TANK, Polymorphism, Single Nucleotide, NF-κB, alcohol, anxiety, insular cortex, Cohort Studies, Translational Research, Biomedical, Animals, Humans, ddc:610, Genetic Association Studies, Adaptor Proteins, Signal Transducing, Aged, Mice, Knockout, Neurosciences, NF-kappa B, Brain, Experimental Psychology, 1702 Cognitive Science, Original Articles, DNA Methylation, Middle Aged, Mice, Inbred C57BL, Female, 1109 Neurosciences, Neurovetenskaper
Abstract

Alcohol abuse is a major public health problem worldwide. Understanding the molecular mechanisms that control regular drinking may help to reduce hazards of alcohol consumption. While immunological mechanisms have been related to alcohol drinking, most studies reported changes in immune function that are secondary to alcohol use. In this report, we analyse how the gene "TRAF family member-associated NF-kappa B activator" (TANK) affects alcohol drinking behavior. Based on our recent discovery in a large GWAS dataset that suggested an association of TANK, SNP rs197273, with alcohol drinking, we report that SNP rs197273 in TANK is associated both with gene expression (P = 1.16 x 10(-19)) and regional methylation (P = 5.90 x 10(-25)). A tank knock out mouse model suggests a role of TANK in alcohol drinking, anxiety-related behavior, as well as alcohol exposure induced activation of insular cortex NF-kappa B. Functional and structural neuroimaging studies among up to 1896 adolescents reveal that TANK is involved in the control of brain activity in areas of aversive interoceptive processing, including the insular cortex, but not in areas related to reinforcement, reward processing or impulsiveness. Our findings suggest that the cortical neuroimmune regulator TANK is associated with enhanced aversive emotional processing that better protects from the establishment of alcohol drinking behavior.

Published
2018

13. The Cortical Neuroimmune Regulator TANK Affects Emotional Processing and Enhances Alcohol Drinking: A Translational Study

Author

Müller, Christian P, primary, Chu, Congying, additional, Qin, Liya, additional, Liu, Chunyu, additional, Xu, Bing, additional, Gao, He, additional, Ruggeri, Barbara, additional, Hieber, Saskia, additional, Schneider, Julia, additional, Jia, Tianye, additional, Tay, Nicole, additional, Akira, Shizuo, additional, Satoh, Takashi, additional, Banaschewski, Tobias, additional, Bokde, Arun L W, additional, Bromberg, Uli, additional, Büchel, Christian, additional, Quinlan, Erin Burke, additional, Flor, Herta, additional, Frouin, Vincent, additional, Garavan, Hugh, additional, Gowland, Penny, additional, Heinz, Andreas, additional, Ittermann, Bernd, additional, Martinot, Jean-Luc, additional, Martinot, Marie-Laure Paillère, additional, Artiges, Eric, additional, Lemaitre, Herve, additional, Nees, Frauke, additional, Papadopoulos Orfanos, Dimitri, additional, Paus, Tomáš, additional, Poustka, Luise, additional, Millenet, Sabina, additional, Fröhner, Juliane H, additional, Smolka, Michael N, additional, Walter, Henrik, additional, Whelan, Robert, additional, Bakalkin, Georgy, additional, Liu, Yun, additional, Desrivières, Sylvane, additional, Elliott, Paul, additional, Eulenburg, Volker, additional, Levy, Daniel, additional, Crews, Fulton, additional, and Schumann, Gunter, additional

Published
2019
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15. Neuroimmune Function and the Consequences of Alcohol Exposure

Author

Vetreno, Ryan, Qin, Liya, Boyadjieva, Nadka, Crews, Fulton, Sarkar, Dipak, and Zou, Jian

Abstract

Induction of neuroimmune genes by binge drinking increases neuronal excitability and oxidative stress, contributing to the neurobiology of alcohol dependence and causing neurodegeneration. Ethanol exposure activates signaling pathways featuring high-mobility group box 1 and Toll-like receptor 4 (TLR4), resulting in induction of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells, which regulates expression of several cytokine genes involved in innate immunity, and its target genes. This leads to persistent neuroimmune responses to ethanol that stimulate TLRs and/or certain glutamate receptors (i.e., N-methyl-d-aspartate receptors). Alcohol also alters stress responses, causing elevation of peripheral cytokines, which further sensitize neuroimmune responses to ethanol. Neuroimmune signaling and glutamate excitotoxicity are linked to alcoholic neurodegeneration. Models of alcohol abuse have identified significant frontal cortical degeneration and loss of hippocampal neurogenesis, consistent with neuroimmune activation pathology contributing to these alcohol-induced, long-lasting changes in the brain. These alcohol-induced long-lasting increases in brain neuroimmune-gene expression also may contribute to the neurobiology of alcohol use disorder.

Published
2015
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