Erqun Song

Southwest University

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Yang Song

Research Center for Eco-Environmental Sciences

138

Zixuan Liu

Institute of Agricultural Resources and Regional Planning

Bingwei Yang

Chinese Academy of Medical Sciences & Peking Union Medical College

Xiaomin Xia

South China Sea Institute Of Oceanology

Juanli Fu

Southwest University

Chuanyang Su

Southwest University

Xiaokang Zhu

Southwest University

Xiufang Song

Chinese Academy of Sciences

Weihong Tan

Shanghai Jiao Tong University

Qiong Shi

Bioscience (China)

Cooperative Institutions

Southwest University

125

Chinese Academy of Sciences

University of Chinese Academy of Sciences

Wuhan University

Sun Yat-sen University

Hunan University

Sichuan University

Chinese Academy of Medical Sciences & Peking Union Medical College

Huazhong University of Science and Technology

Shanghai Jiao Tong University

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Long-term pulmonary iron oxide nanoparticles exposure disrupts hepatic iron-lipid homeostasis and increases plaque vulnerability in ApoE−/− mice

Environmental Pollution (2023)

Ziyi Yan Zixuan Liu Bingwei Yang Xiangyu Zhu Erqun Song

Homeostasis

Apolipoprotein E

Dyslipidemia

10.1016/j.envpol.2023.122905

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Citations (2)

Delivery of Ultrasmall Nanoparticles to the Cytosolic Compartment of Pyroptotic J774A.1 Macrophages via GSDMD^Nterm Membrane Pores

ACS Applied Materials & Interfaces (2021)

Di Wu Xiangyu Zhu Jian Ao Erqun Song Yang Song

Endosome capture is a major physiological barrier to the successful delivery of nanomedicine. Here, we found a strategy to deliver ultrasmall nanoparticles (<10 nm) to the cytosolic compartment of pyroptotic cells with spontaneous endosomal escape. To mimic pathological pyroptotic cells, J774A.1 macrophages were stimulated with lipopolysaccharide (LPS) plus nigericin (Nig) or adenosine triphosphate (ATP) to form specific gasdermin D protein-driven membrane pores at an N-terminal domain (GSDMDNterm). Through GSDMDNterm membrane pores, both anionic and cationic nanoparticles (NPs) with diameters less than 10 nm were accessed into the cytosolic compartment of pyroptotic cells in an energy- and receptor-independent manner, while NPs larger than the size of GSDMDNterm membrane pores failed to enter pyroptotic cells. NPs pass through GSDMDNterm membrane pores via free diffusion and then access into the cytoplasm of pyroptotic cells in a microtubule-independent manner. Interestingly, we found that LPS-primed NPs may act as Trojan horse, deliver extracellular LPS into normal cells through endocytosis, and in turn induce GSDMDNterm membrane pores, which facilitate further internalization of NPs. This study presented a straightforward method of distinguishing normal and pyroptotic cells through GSDMD membrane pores, implicating their potential application in monitoring the delivery of desired nanomedicines in pyroptosis-related diseases and conditions.

Nigericin

Pyroptosis

10.1021/acsami.1c17382

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Citations (10)

Copper oxide nanoparticles induce cuproptosis and ferroptosis through mitochondrial concatenation

Environmental Science Nano (2024)

Muran Jiang Xiaoqi Tao Yingxin Pang Zongmin Qin Erqun Song

Our work suggested that cuproptosis serves as a key toxic mechanism of CuO NPs, damaging mitochondria to induce ferroptosis by disrupting mitochondrial membrane lipid synthesis.

Concatenation (mathematics)

Copper oxide

10.1039/d4en00455h

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Citations (2)

Enzyme-activated apoptotic bodies-encapsulated NSET biomimetic probe for wash-free detection of intracellular pathogen in synovial fluid and monitoring therapy effect of septic arthritis

Chemical Engineering Journal (2024)

Yun Yang Mingrong Wu Yaqing Zhang Lin Wang Yang Song

10.1016/j.cej.2024.149539

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Citations (2)

Polybrominated Diphenyl Ethers Quinone Induced Parthanatos-like Cell Death through a Reactive Oxygen Species-Associated Poly(ADP-ribose) Polymerase 1 Signaling

Chemical Research in Toxicology (2018)

Wenjing Dong Bingwei Yang Yawen Wang Yuan Jia Yunqi Fan

Polybrominated diphenyl ethers (PBDEs) are emerging organic environmental pollutants, which were accused of various toxic effects. Here, we studied the role of a potential PBDEs quinone metabolite, PBDEQ, on cytotoxicity, oxidative DNA damage, and the alterations of signal cascade in HeLa cells. PBDEQ exposure leads to reactive oxygen species (ROS) accumulation, mitochondrial membrane potential (MMP) loss, lactate dehydrogenase (LDH) release, increasing terminal transferase-mediated dUTP-biotin nick end labeling (TUNEL) positive foci, and the elevation of apoptosis rate. Furthermore, we showed PBDEQ exposure result in increased DNA migration, micronucleus frequency, and the promotion of 8-OHdG and phosphorylation of histone H2AX (γ-H2AX) levels. Mechanism study indicated that PBDEQ caused poly(ADP-ribose) polymerase 1 (PARP-1) activation and apoptosis-inducing factor (AIF) nuclear translocation. All together, these results confirmed the occurrence of parthanatos-like cell death upon PBDEQ exposure.

PARP1

HeLa

10.1021/acs.chemrestox.8b00168

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Citations (18)

Activating Transcription Factor 4 (ATF4)-ATF3-C/EBP Homologous Protein (CHOP) Cascade Shows an Essential Role in the ER Stress-Induced Sensitization of Tetrachlorobenzoquinone-Challenged PC12 Cells to ROS-Mediated Apoptosis via Death Receptor 5 (DR5) Signaling

Chemical Research in Toxicology (2016)

Zixuan Liu Qiong Shi Xiufang Song Yuxin Wang Yawen Wang

Tetrachlorobenzoquinone (TCBQ) is a downstream metabolite of pentachlorophenol (PCP). Previously, we demonstrated that TCBQ caused cytotoxicity due to mitochondrial-related apoptosis. Here, we confirmed the upregulation of death receptor 5 (DR5) followed by the construction of the death-inducing signaling complex (DISC). We also detected the activation of the caspase cascade, which was correlated with TCBQ-induced apoptotic cell death in PC12 cells. The upregulation of DR5 included transcriptional activation and de novo protein synthesis in response to TCBQ. We also identified the endoplasmic reticulum (ER) as a new target for the TCBQ challenge in PC12 cells. The protein kinase R-like ER kinase/eukaryotic translation initiation factor 2α (PERK/eIF2α)-mediated activating transcription factor 4 (ATF4)-ATF3-C/EBP homologous protein (CHOP) signaling pathway contributed to the process of TCBQ-induced ER stress. Blocking ATF4, ATF3, or CHOP signaling by gene silencing technology resulted in decreased cell apoptosis after exposure to TCBQ. Finally, NAC ameliorated TCBQ-induced apoptosis and ER stress, which illustrated that TCBQ-induced apoptosis is somehow ROS-dependent. In summary, this study provided important mechanistic insight into how TCBQ utilizes ER stress-related signaling to exhibit pro-apoptotic activity in PC12 cells.

ATF4

Activating transcription factor

Integrated stress response

10.1021/acs.chemrestox.6b00181

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Citations (53)

One-Step Determination of Alkaline Phosphatase in Human Serum Based on Manganese (IV) Dioxide/Manganese (II)-Mediated Nuclear Magnetic Resonance (NMR) Relaxation

Analytical Letters (2022)

Qin Luo Zhenping Gao Qinni Xiao Erqun Song

Alkaline phosphatase (ALP) is a significant biomarker of diseases, such as osteoblastic bone cancer, hepatitis, and myeloma, and hence its determination is essential and important. MnO2/Mn2+ conversion-based magnetic relaxation sensing was developed to directly determine ALP in blood. In the presence of ALP, 2-phospho-L-ascorbic acid trisodium salt was catalyzed to produce ascorbic acid (AA), which reduced MnO2 to Mn2+, causing transverse relaxation time (T2) decay. A linear relationship of ALP from 5 mU·L−1 to 500 mU·L−1 with T2 signal and a low limit of detection (LOD) of 3.32 mU·L−1 were obtained using the optimized conditions of 200 µM of ascorbic acid-phosphate (AAP), 10 µg·mL−1 of MnO2, 37 °C, pH 7.4, and a 30 min reaction time. When directly measuring ALP in serum with the proposed method, the recoveries were from 99.2% to 101.3%, in accordance with values obtained by a commercial assay. In conclusion, a sensitive one-step method for ALP in complex samples was established which has potential for clinical applications.

10.1080/00032719.2022.2076108

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Citations (3)

A pH-responsive magnetic resonance tuning probe for precise imaging of bacterial infection in vivo

Acta Biomaterialia (2023)

Linyao Li Maojuan Liu Siyu Deng Xiaokang Zhu Yang Song

10.1016/j.actbio.2023.04.009

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Citations (8)

Self‐Assembled Aptamer‐Based Drug Carriers for Bispecific Cytotoxicity to Cancer Cells

Chemistry - An Asian Journal (2012)

Guizhi Zhu Ling Meng Mao Ye Liu Yang Kwame Sefah

Abstract Monovalent aptamers can deliver drugs to target cells by specific recognition. However, different cancer subtypes are distinguished by heterogeneous biomarkers and one single aptamer is unable to recognize all clinical samples from different patients with even the same type of cancers. To address heterogeneity among cancer subtypes for targeted drug delivery, as a model, we developed a drug carrier with a broader recognition range of cancer subtypes. This carrier, sgc8c‐sgd5a (SD), was self‐assembled from two modified monovalent aptamers. It showed bispecific recognition abilities to target cells in cell mixtures; thus broadening the recognition capabilities of its parent aptamers. The self‐assembly of SD simultaneously formed multiple drug loading sites for the anticancer drug doxorubicin (Dox). The Dox‐loaded SD (SD–Dox) also showed bispecific abilities for target cell binding and drug delivery. Most importantly, SD–Dox induced bispecific cytotoxicity in target cells in cell mixtures. Therefore, by broadening the otherwise limited recognition capabilities of monovalent aptamers, bispecific aptamer‐based drug carriers would facilitate aptamer applications for clinically heterogeneous cancer subtypes that respond to the same cancer therapy.

Aptamer

Targeted drug delivery

10.1002/asia.201101060

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Citations (64)

Copper oxide nanoparticles induce non-alcoholic fatty liver disease by disrupting bile acid homeostasis and perturbing the intestinal microbial homeostasis

Journal of Hazardous Materials (2024)

Muran Jiang Xiaoqi Tao Yingxin Pang Zongmin Qin Erqun Song

Homeostasis

10.1016/j.jhazmat.2024.136416

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Citations (0)