Yudong Ji

ORCID: 0000-0003-1638-5497
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Research Areas
  • Extracellular vesicles in disease
  • MicroRNA in disease regulation
  • Immune cells in cancer
  • Immune Response and Inflammation
  • Galectins and Cancer Biology
  • Gut microbiota and health
  • Spine and Intervertebral Disc Pathology
  • Immune Cell Function and Interaction
  • Adipose Tissue and Metabolism
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Inflammasome and immune disorders
  • Cancer-related molecular mechanisms research
  • Cardiovascular Disease and Adiposity
  • Medical Imaging and Analysis
  • Peptidase Inhibition and Analysis
  • Liver Disease Diagnosis and Treatment
  • Signaling Pathways in Disease
  • Respiratory Support and Mechanisms
  • Neonatal Respiratory Health Research
  • Management of metastatic bone disease
  • Macrophage Migration Inhibitory Factor
  • Carbon and Quantum Dots Applications
  • Luminescence and Fluorescent Materials
  • Adipokines, Inflammation, and Metabolic Diseases
  • Protein Kinase Regulation and GTPase Signaling

Huazhong University of Science and Technology
2013-2024

Union Hospital
2003-2024

Xinxiang Medical University
2024

Union Hospital
2022

University of California, San Diego
1990-2022

Wuhan Union Hospital
2022

Tongji Hospital
2020

Weifang People's Hospital
2014

The intracellular distribution of regulatory molecules may provide a mechanism for controlling gene expression. subcellular location cAMP-dependent protein kinase was analyzed in living cells by microinjection and catalytic subunits labeled with fluorescein. Following microinjection, type I holoenzyme found the cytoplasm remained there up to 4 hr. Upon dissociation 8-bromo-cAMP, free subunit appeared nucleus while cytoplasm. Similarly, purified transported absence elevated cAMP following its...

10.1073/pnas.87.24.9595 article EN Proceedings of the National Academy of Sciences 1990-12-01

Acute lung injury (ALI) is characterized by inflammation and diffuse infiltration of neutrophils. Neutrophil apoptosis recognized as an important control point in the resolution inflammation. Maresin 1 (MaR1) a new docosahexaenoic acid-derived proresolving agent that promotes However, its function neutrophil unknown. In this study, isolated human neutrophils were incubated with MaR1, pan-caspase inhibitor z-VAD-fmk, lipopolysaccharide (LPS) to determine mechanism apoptosis. was induced...

10.1097/shk.0000000000000434 article EN Shock 2015-07-21

Various microbial products leaked from gut lumen exacerbate tissue inflammation and metabolic disorders in obesity. Vsig4+ macrophages are key players preventing infiltration of bacteria their into host tissues. However, roles islet the communication between microbiota β cells pathogenesis obesity-associated abnormalities unknown. Here, we find that bacterial DNAs enriched individuals with Intestinal DNA-containing extracellular vesicles (mEVs) readily pass through obese barrier deliver...

10.1038/s41467-022-28239-2 article EN cc-by Nature Communications 2022-01-28

Abstract Aim Low‐grade inflammation is the hallmark of non‐alcoholic fatty liver diseases (NAFLD) and steatohepatitis (NASH). The leakage microbiota‐derived products can contribute to during NAFLD/NASH development. Here, we assessed roles gut microbial DNA‐containing extracellular vesicles (mEVs) in regulating cellular abnormalities course NAFLD/NASH. Methods We performed studies with Vsig4 −/− , C3 cGAS their wild‐type littermate mice. Vsig4+ macrophage population bacterial DNA abundance...

10.1111/apha.13827 article EN Acta Physiologica 2022-05-02

Obesity induces an adaptive expansion of β cell mass and insulin secretion abnormality. Expansion adipose tissue macrophages (ATMs) is a hallmark obesity. Here, we assessed novel role ATMs in mediating obesity-induced adaptation through the release miRNA-containing extracellular vesicles (EVs). In both vivo vitro experiments, show that ATM EVs derived from obese mice notably suppress enhance proliferation. We also observed similar phenotypes human islets after EV treatment. Importantly,...

10.3390/cells10092451 article EN cc-by Cells 2021-09-17

Lung fibrosis is an aggressive disease with uncontrolled fibrotic response and no effective therapeutic treatment. Epithelial-to-mesenchymal transition (EMT) has been proved to be important pathological feature in lung fibrosis. In this study, we investigated whether MaR1, a kind of proresolving lipid mediators, could inhibit TGF-β1-induced EMT vitro vivo. mouse type II alveolar epithelial cells were treated different does MaR1 for 30 min exposed TGF-β1 48 h. vivo C57BL/6 mice administered...

10.1097/shk.0000000000000446 article EN Shock 2015-07-21

Gut microbiota-derived extracellular vesicles (mEVs) are reported to regulate inflammatory response by delivering bacterial products into host cells. The complement receptor of the immunoglobulin superfamily macrophages (CRIg+ Mφ) could clear invading bacteria and their derivatives. Here, we investigate role CRIg+ Mφ mechanism which mEVs intestinal inflammation. We found that it is exacerbated in IBD patients colitis mice mEVs' leakage from disturbed gut microbiota, enriching microbial DNA...

10.1080/19490976.2024.2379633 article EN cc-by-nc Gut Microbes 2024-07-18

Background Obesity is an established risk factor for hypertension. Although obesity-induced gut barrier breach leads to the leakage of various microbiota-derived products into host circulation and distal organs, roles microbiota in mediating development obesity-associated adrenomedullary disorders hypertension have not been elucidated. We seek explore impacts microbial DNA enrichment on inducing obesity-related abnormalities Methods Results was accompanied by remarkable bacterial...

10.1161/jaha.121.024561 article EN cc-by-nc-nd Journal of the American Heart Association 2022-02-03

Pulmonary fibrosis is an aggressive end‑stage disease. Transforming growth factor‑β1 (TGF‑β1) mediates lung fibroblast activation and essential for the progress of pulmonary fibrosis. BML‑111, a lipoxinA4 (LXA4) receptor (ALX) agonist, has been reported to possess anti‑fibrotic properties. The present study aimed elucidate whether BML‑111 inhibits TGF‑β1‑induced mouse embryo (NIH3T3 cell line) in vitro bleomycin (BLM)‑induced vivo. In experiments demonstrated that treatment NIH3T3 viability...

10.3892/ijmm.2018.3914 article EN cc-by-nc-nd International Journal of Molecular Medicine 2018-10-02

To investigate whether visceral metastases have a significant impact on survival in patients with metastasis-related spinal cord compression (MSCC), and to determine the difference prognosis between without metastases.Three institutional databases were searched identify all who had undergone surgery for March 2002 June 2010. Data patient characteristics including pre- post-operative medical conditions, collected from records or by telephone follow-up. Survival data obtained either searching...

10.1111/os.12465 article EN cc-by Orthopaedic Surgery 2019-04-15

Abstract Obesity induces an adaptive expansion of β cell mass and insulin secretion abnormality. Here, we explore a novel role adipose tissue macrophages (ATMs) in mediating obesity-induced function proliferation through releasing miRNA-containing extracellular vesicles (EVs). ATM EVs derived from obese mice notably suppress both vivo vitro experiments, whereas there are more proliferating cells the islets treated with EVs. Depletion miRNAs blunts ability to regulate responses. miR-155,...

10.1101/2020.06.12.148809 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2020-06-13

Objective To evaluate the effects of aspirin-triggered lipoxin A4 (ATL) on lipopolysaccharide (LPS)-induced acute lung injury in mice.Methods Thirty male SPF BALB/C mice,aged 10-12 weeks,weighing 25-30 g,were randomly assigned into 3 groups (n =10 each):normal saline group (group NS),LPS and ATL groups.ATL 0.1 ml was injected via tail vein 1 h after intra-tracheal instillation mg/kg LPS group.In group,ATL 0.2 LPS.At 24 instillation,the mice were sacrificed.Bronchoalveolar lavage fluid...

10.3760/cma.j.issn.0254-1416.2013.05.020 article EN 2013-05-20

10.1016/s0301-5629(03)00706-3 article EN Ultrasound in Medicine & Biology 2003-05-01
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