G. Zhang

Qilu Hospital of Shandong University

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Liyan Xue

Chinese Academy of Medical Sciences & Peking Union Medical College

Z. Zhang

University of Liverpool

Chunli Zhang

Chinese Academy of Medical Sciences & Peking Union Medical College

Qi Xue

Chinese Academy of Medical Sciences & Peking Union Medical College

Nan Sun

Chinese Academy of Medical Sciences & Peking Union Medical College

Qixian Zeng

Peking Union Medical College Hospital

Mo Wang

Peking University

Shugeng Gao

Chinese Academy of Medical Sciences & Peking Union Medical College

Haiping Yang

Chongqing Medical University

Bin Yang

Capital Medical University

Cooperative Institutions

Chinese Academy of Medical Sciences & Peking Union Medical College

Peking Union Medical College Hospital

Qilu Hospital of Shandong University

National Clinical Research

Sichuan University

Capital Medical University

Sun Yat-sen University

Shanxi Medical University

Huazhong University of Science and Technology

Wuhan University

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Protein kinase R is highly expressed in dermatomyositis and promotes interferon-beta-induced muscle damage

Annals of the Rheumatic Diseases (2024)

G. Zhang Lining Zhang Dandan Zhao Xiaoyu Liu Wei Li

Objectives Dermatomyositis (DM) has been consistently linked to the type I interferon (IFN-I) pathway. However, the precise pathogenesis remains incompletely elucidated. We aimed to explore potential molecular mechanisms and identify promising therapeutic targets in DM. Methods We employed bioinformatics analysis to investigate molecular signatures, aiming to shed light on the pathogenesis of DM. The expression of protein kinase R (PKR) in DM muscle tissues was determined by real-time quantitative PCR, western blot and immunohistochemistry (IHC) analysis. We then assessed the sensitivity and specificity of sarcoplasmic PKR expression by IHC in a consecutive DM cohort and other diseases in this retrospective study. Furthermore, IFN-β was used to stimulate myoblasts and myotubes, and the relationship between PKR and IFN-β-induced pathogenic molecules was investigated in vitro. Results Bioinformatics analysis indicated two primary pathological processes: viral infection and the IFN-I signalling pathway. We subsequently verified that PKR was notably expressed in the cytoplasm of myofibers in DM patients. The sensitivity and specificity of sarcoplasmic PKR expression in DM were 84.6% and 97.6%, respectively. In vitro studies revealed that IFN-β upregulates the expression of PKR, along with several molecules associated with DM muscle damage. Conversely, inhibiting PKR has been shown to downregulate IFN-β-induced pathogenic molecules in both myoblasts and myotubes. Conclusions We observed that PKR exhibits specific expression in the cytoplasm of DM muscle and inhibiting PKR ameliorates IFN-β-induced muscle damage in vitro. These findings provide insights into the diagnostic and therapeutic roles of PKR in DM.

Protein kinase R

EIF-2 kinase

Pathogenesis

10.1136/ard-2024-226057

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Molecular cloning and expression of interleitkin-6 in Escherichia coli

Toxicon (1997)

H. Liu Tian Xie G. Zhang Xiaozhong Peng Qiangming Sun

Cloning (programming)

10.1016/s0041-0101(97)84763-0

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14P High CMTM6 and PD-L1 co-expression predict metastasis and poor prognosis in oesophageal squamous cell carcinoma

Annals of Oncology (2020)

Yufeng Luo Chunli Zhang Z. Zhang G. Zhang Liyan Xue

10.1016/j.annonc.2020.10.499

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IL-23 Activated γδ T Cells Affect Th17 Cells and Regulatory T Cells by Secreting IL-21 in Children with Primary Nephrotic Syndrome

Scandinavian Journal of Immunology (2017)

Luo Zhang Jun Yan Bin Yang G. Zhang Mo Wang

This study (1) analysed the percentage of γδ T cells, γδ T cell subsets, Th17 cells and regulatory T cells (Treg cells) and (2) determined the role of IL-23 in primary nephrotic syndrome (PNS) patients with active disease and in remission. Eighty-four patients with PNS and 51 healthy age-matched controls were included in this study. The percentage of γδ T cells, γδ T cell subsets, Th17 cells and Treg cells in peripheral blood mononuclear cells (PBMCs) were analysed by fluorescence-activated cell sorting. PMBCs from PNS patients with active disease were cultured in the presence of IL-23, IL-23 and an IL-23 antagonist, or IL23 and an anti-IL-21 monoclonal antibody (mAb). The percentage of γδ T cells, IL-23R+ γδ T cells and IL-17+ γδ T cells were significantly increased in PNS patients with active disease. There was a positive correlation between the percentage of γδ T cells, IL-23R+ γδ T cells, IL-17+ γδ T cells and the Th17/Treg ratio. IL-23 increased the percentage of γδ T cells and Th17 cells and decreased the percentage of Treg cells in PBMCs isolated from PNS patients with active disease. Anti-IL-21 mAb reduced the percentage of γδ T cells and Th17 cells, but increased the percentage of Treg cells. γδ T cells, IL-17+ γδ T cells and IL-23R+ γδ T cells may be involved in the pathogenesis of paediatric PNS by modulating the balance of Th17/Treg cells. γδ T cells may cause an imbalance in Th17/Treg cells by secreting IL-21 in the presence of IL-23.

Interleukin 3

10.1111/sji.12629

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20P Quantitative whole slide assessment of CD8+ tumour-infiltrating lymphocytes in small cell esophageal carcinoma in relation to clinical outcome

Annals of Oncology (2020)

Z. Zhang Chunli Zhang G. Zhang Liyan Xue Qixian Zeng

Tumor-infiltrating lymphocytes

10.1016/j.annonc.2020.10.505

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Induction of G1 arrest and differentiation in MDA-MB-231 breast cancer cell by boehmeriasin A, a novel compound from plant

International Journal of Gynecological Cancer (2006)

Juan Yan Dan Luo Ya Luo Xuefei Gao G. Zhang

Boehmeriasin A is a new phenanthroquinolizidine alkaloid recently isolated from the Boehmeria siamensis Craib (Urticaceae). In vitro biological activity assay demonstrated that this novel compound has wide-range, strong antitumor activity. This study is aimed to determine the effects of boehmeriasin A on breast cancer cell (MDA-MB-231 cell line). Proliferation assay and fluorescence activated cell sorter (FACS) showed that cell growth inhibition and G1 phase arrest of cell cycle were caused by boehmeriasin A. The concentrations resulting in total and 50% growth inhibition are 0.007 and 0.0035 μg/mL, respectively. Exposed in 0.007 μg/mL boehmeriasin A for 12 h, the G1 phase cell percent increased from 44.8% pre–drug treatment to 66.3%. Consistent with G1 arrest and cell growth inhibition, cyclin E2 and cyclin D1 messenger RNA expression in the cell was down-regulated with drug treatment. Then, few apoptotic cells were detected, and most other cells underwent differentiation, which is characterized by specific changes in cell morphology, lots of lipid droplet accumulation, and increasing expression of adipocyte differentiation–related protein. The result first demonstrates that boehmeriasin A potently inhibits the proliferation of breast cancer cell MDA-MB-231 via the G1 phase cell cycle arrest and differentiation induction, and as such, may be considered as candidate chemotherapeutic and/or chemopreventive agent for breast cancer.

G1 phase

Growth inhibition

Cyclin E

Cyclin B1

Cyclin A

10.1136/ijgc-00009577-200601000-00027

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