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Your search keyword '"Yucun Chen"' showing total 2 results
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2 results on '"Yucun Chen"'

1. Comparative proteomics in captive giant pandas to identify proteins involved in age-related cataract formation

Author

Yuyan You, Chao Bai, Wei Wang, Tongtong Zhan, Xin Hu, Feier Hao, Maohua Xia, Yan Liu, Tao Ma, Yanhui Liu, Changming Zheng, Tianchun Pu, Yizhuo Zhang, Yanping Lu, Nan Ding, Jing Li, Yanqiang Yin, Yucun Chen, Liqin Wang, Jun Zhou, Lili Niu, Yunfang Xiu, Yan Lu, Ting Jia, Xuefeng Liu, and Chenglin Zhang

Subjects
Medicine, Science
Abstract

Abstract Approximately 20% of aged captive giant pandas (Ailuropoda melanoleuca) have cataracts that impair their quality of life. To identify potential biomarkers of cataract formation, we carried out a quantitative proteomics analysis of 10 giant pandas to find proteins differing in abundance between healthy and cataract-bearing animals. We identified almost 150 proteins exceeding our threshold for differential abundance, most of which were associated with GO categories related to extracellular localization. The most significant differential abundance was associated with components of the proteasome and other proteins with a role in proteolysis or its regulation, most of which were depleted in pandas with cataracts. Other modulated proteins included components of the extracellular matrix or cytoskeleton, as well as associated signaling proteins and regulators, but we did not find any differentially expressed transcription factors. These results indicate that the formation of cataracts involves a complex post-transcriptional network of signaling inside and outside lens cells to drive stress responses as a means to address the accumulation of protein aggregates triggered by oxidative damage. The modulated proteins also indicate that it should be possible to predict the onset of cataracts in captive pandas by taking blood samples and testing them for the presence or absence of specific protein markers.

Published
2023
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2. Increased Non-MAIT CD161(+)CD8(+) T Cells Display Pathogenic Potential in Chronic HBV Infection

Author

Yu Liu, Wei Wang, Peng Zhu, Xue Cheng, Mi Wu, Haoquan Zhang, Yiqing Chen, Yucun Chen, Zhihui Liang, Xiongwen Wu, and Xiufang Weng

Subjects
Hepatology, Gastroenterology, Original Research
Abstract

BACKGROUND & AIMS: CD161-expressing CD8(+) T cells consist of mucosal-associated invariant T cells with semi-invariant T-cell receptor (TCR) use and non–mucosal-associated invariant T CD161(+)CD8(+) T cells with polyclonal TCR repertoire. Although CD161(+)CD8(+) T cells are enriched in liver and embrace hepatitis B virus (HBV)-specific T cells in chronic hepatitis B (CHB) patients, their roles in disease progression remain poorly understood. This study aimed to decipher their profiling and dynamic changes during chronic HBV infection. METHODS: Blood samples from 257 CHB patients and nontumor liver specimens from 73 HBV-positive patients were analyzed for CD161(+)CD8(+) T-cell characterization by flow cytometry, TCR repertoire determination, transcriptomic analyses, and cell experiments. RESULTS: CD161(+)CD8(+) T cells were increased and hyperactivated in patients, while positive correlation between the CD161(+)CD8(+) T-cell ratio and HBV-DNA level suggested this was insufficient to control HBV replication. The overlap of complementarity determining region 3 sequences supported the switch between CD161(-)CD8(+) and CD161(+)CD8(+) populations. Although CD161(+)CD8(+) T cells were endowed with innateness phenotype and enhanced antiviral capacity, the population from patients had impaired type I cytokine production, and increased interleukin 17 and granzyme B secretion. The increased CD161(+)CD8(+) T cells and their increased granzyme B secretion correlated positively with inflammation-associated liver injury. Hepatic CD161(+)CD8(+) T cells showed neutrophil-related pathogenic potential because they had increased transcript signatures and proinflammatory cytokine production in neutrophil recruitment- and response-related pathways that changed consistently in the injured liver. CONCLUSIONS: Our results highlight the reduced antiviral potency but increased pathogenic potential of CD161(+)CD8(+) T cells in CHB patients, supporting CD161 expression as a marker of pathogenic CD8(+) T subset and the intervention target for liver injury.

Published
2023

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