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Article ; Online: Ubiquitin-specific peptidase 25 exacerbated osteoarthritis progression through facilitating TXNIP ubiquitination and NLRP3 inflammasome activation.

Sui, Jie / Dai, Fei / Shi, Jiusheng / Zhou, Changcheng

Journal of orthopaedic surgery and research

2023 Volume 18, Issue 1, Page(s) 762

Abstract: Several members of the ubiquitin-specific proteases (USPs) family have been revealed to regulate the progression of osteoarthritis (OA). The current study aimed to investigate the role and the underlying mechanism of USP25 in IL-1β-induced chondrocytes ... ...

Abstract	Several members of the ubiquitin-specific proteases (USPs) family have been revealed to regulate the progression of osteoarthritis (OA). The current study aimed to investigate the role and the underlying mechanism of USP25 in IL-1β-induced chondrocytes and OA rat model. It was discovered that IL-1β stimulation upregulated USP25, increased ROS level, and suppressed cell viability in rat chondrocytes. Besides, USP25 knockdown alleviated IL-1β-induced injury by decreasing ROS level, attenuating pyroptosis, and downregulating the expression of IL-18, NLRP3, GSDMD-N, active caspase-1, MMP-3, and MMP-13. Furthermore, we discovered that USP25 affected the IL-1β-induced injury in chondrocytes in a ROS-dependent manner. Moreover, USP25 was revealed to interact with TXNIP, and USP25 knockdown increased the ubiquitination of TXNIP. The pro-OA effect of USP25 abundance could be overturned by TXNIP suppression in IL-1β-induced chondrocytes. Finally, in vivo experiment results showed that USP25 inhibition alleviated cartilage destruction in OA rats. In conclusion, we demonstrated that USP25 stimulated the overproduction of ROS to activate the NLRP3 inflammasome via regulating TXNIP, resulting in increased pyroptosis and inflammation in OA.
MeSH term(s)	Animals ; Rats ; Cell Cycle Proteins ; Inflammasomes/metabolism ; Inflammation/metabolism ; Interleukin-1beta/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Osteoarthritis/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Cell Cycle Proteins ; Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Reactive Oxygen Species ; TXNIP protein, rat ; Nlrp3 protein, rat
Language	English
Publishing date	2023-10-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2252548-8
ISSN	1749-799X ; 1749-799X
ISSN (online)	1749-799X
ISSN	1749-799X
DOI	10.1186/s13018-023-04083-y
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Article: Recent Advances in Understanding the Role of IKKβ in Cardiometabolic Diseases.

Hernandez, Rebecca / Zhou, Changcheng

Frontiers in cardiovascular medicine

2021 Volume 8, Page(s) 752337

Abstract: Cardiometabolic diseases, including cardiovascular disease, obesity, and diabetes, are the leading cause of mortality and morbidity worldwide. Cardiometabolic diseases are associated with many overlapping metabolic syndromes such as hypertension, ... ...

Abstract	Cardiometabolic diseases, including cardiovascular disease, obesity, and diabetes, are the leading cause of mortality and morbidity worldwide. Cardiometabolic diseases are associated with many overlapping metabolic syndromes such as hypertension, hyperlipidemia, insulin resistance, and central adiposity. However, the underlying causes of cardiometabolic diseases and associated syndromes remain poorly understood. Within the past couple of decades, considerable progresses have been made to understand the role of inflammatory signaling in the pathogenesis of cardiometabolic diseases. The transcription factor, NF-κB, a master regulator of the innate and adaptive immune responses, is highly active in cardiometabolic diseases. IκB kinase β (IKKβ), the predominant catalytic subunit of the IKK complex, is required for canonical activation of NF-κB, and has been implicated as the critical molecular link between inflammation and cardiometabolic diseases. Recent studies have revealed that IKKβ has diverse and unexpected roles in mediating adiposity, insulin sensitivity, glucose homeostasis, vascular function, and atherogenesis through complex mechanisms. IKKβ has been demonstrated as a critical player in the development of cardiometabolic diseases and is implicated as a promising therapeutic target. This review summarizes current knowledge of the functions of IKKβ in mediating the development and progression of cardiometabolic diseases.
Language	English
Publishing date	2021-12-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2781496-8
ISSN	2297-055X
ISSN	2297-055X
DOI	10.3389/fcvm.2021.752337
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Article: Novel functions of PXR in cardiometabolic disease.

Zhou, Changcheng

Biochimica et biophysica acta

2016 Volume 1859, Issue 9, Page(s) 1112–1120

Abstract: Cardiometabolic disease emerges as a worldwide epidemic and there is urgent need to understand the molecular mechanisms underlying this chronic disease. The chemical environment to which we are exposed has significantly changed in the past few decades ... ...

Abstract	Cardiometabolic disease emerges as a worldwide epidemic and there is urgent need to understand the molecular mechanisms underlying this chronic disease. The chemical environment to which we are exposed has significantly changed in the past few decades and recent research has implicated its contribution to the development of many chronic human diseases. However, the mechanisms of how exposure to chemicals contributes to the development of cardiometabolic disease are poorly understood. Numerous chemicals have been identified as ligands for the pregnane X receptor (PXR), a nuclear receptor functioning as a xenobiotic sensor to coordinately regulate xenobiotic metabolism via transcriptional regulation of xenobiotic-detoxifying enzymes and transporters. In the past decade, the function of PXR in the regulation of xenobiotic metabolism has been extensively studied by many laboratories and the role of PXR as a xenobiotic sensor has been well-established. The identification of PXR as a xenobiotic sensor has provided an important tool for the study of new mechanisms through which xenobiotic exposure impacts human chronic diseases. Recent studies have revealed novel and unexpected roles of PXR in modulating obesity, insulin sensitivity, lipid homeostasis, atherogenesis, and vascular functions. These studies suggest that PXR signaling may contribute significantly to the pathophysiological effects of many known xenobiotics on cardiometabolic disease in humans. The discovery of novel functions of PXR in cardiometabolic disease not only contributes to our understanding of "gene-environment interactions" in predisposing individuals to chronic diseases but also provides strong evidence to inform future risk assessment for relevant chemicals. This article is part of a Special Issue entitled: Xenobiotic nuclear receptors: New Tricks for An Old Dog, edited by Dr. Wen Xie.
MeSH term(s)	Animals ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Blood Vessels/metabolism ; Blood Vessels/pathology ; Chronic Disease ; Gene Expression Regulation ; Gene-Environment Interaction ; Humans ; Inactivation, Metabolic/genetics ; Insulin Resistance/genetics ; Intestinal Mucosa/metabolism ; Intestines/pathology ; Lipid Metabolism/genetics ; Liver/metabolism ; Liver/pathology ; Obesity/genetics ; Obesity/metabolism ; Obesity/pathology ; Pregnane X Receptor ; Receptors, Steroid/genetics ; Receptors, Steroid/metabolism ; Signal Transduction ; Xenobiotics/administration & dosage ; Xenobiotics/metabolism
Chemical Substances	Pregnane X Receptor ; Receptors, Steroid ; Xenobiotics
Language	English
Publishing date	2016-02-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagrm.2016.02.015
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Article ; Online: Anti-CD47 antibody treatment attenuates liver inflammation and fibrosis in experimental non-alcoholic steatohepatitis models.

Gwag, Taesik / Ma, Eric / Zhou, Changcheng / Wang, Shuxia

Liver international : official journal of the International Association for the Study of the Liver

2022 Volume 42, Issue 4, Page(s) 829–841

Abstract: Background & aims: With the epidemic burden of obesity and metabolic diseases, nonalcoholic fatty liver disease (NAFLD) including steatohepatitis (NASH) has become the most common chronic liver disease in the western world. NASH may progress to ... ...

Abstract	Background & aims: With the epidemic burden of obesity and metabolic diseases, nonalcoholic fatty liver disease (NAFLD) including steatohepatitis (NASH) has become the most common chronic liver disease in the western world. NASH may progress to cirrhosis and hepatocellular carcinoma. Currently, no treatment is available for NASH. Therefore, finding a therapy for NAFLD/NASH is in urgent need. Previously we have demonstrated that mice lacking CD47 or its ligand thrombospondin1 (TSP1) are protected from obesity-associated NALFD. This suggests that CD47 blockade might be a novel treatment for obesity-associated metabolic disease. Thus, in this study, the therapeutic potential of an anti-CD47 antibody in NAFLD progression was determined. Methods: Both diet-induced NASH mouse model and human NASH organoid model were utilized in this study. NASH was induced in mice by feeding with diet enriched with fat, fructose and cholesterol (AMLN diet) for 20 weeks and then treated with anti-CD47 antibody or control IgG for 4 weeks. Body weight, body composition and liver phenotype were analysed. Results: We found that anti-CD47 antibody treatment did not affect mice body weight, fat mass or liver steatosis. However, liver immune cell infiltration, inflammation and fibrosis were significantly reduced by anti-CD47 antibody treatment. In vitro data further showed that CD47 blockade prevented hepatic stellate cell activation and NASH progression in a human NASH organoid model. Conclusion: Collectively, these data suggest that anti-CD47 antibody might be a new therapeutic option for obesity-associated NASH and liver fibrosis.
MeSH term(s)	Animals ; CD47 Antigen ; Diet, High-Fat ; Disease Models, Animal ; Humans ; Liver/pathology ; Liver Cirrhosis/pathology ; Liver Neoplasms/pathology ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease/pathology
Chemical Substances	CD47 Antigen
Language	English
Publishing date	2022-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2102783-3
ISSN	1478-3231 ; 1478-3223
ISSN (online)	1478-3231
ISSN	1478-3223
DOI	10.1111/liv.15182
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Zs.A 1632: Show issues

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Article: Immunomagnetic Delivery of Adipose-Derived Endothelial Progenitor Cells for the Repair of Renal Ischemia-Reperfusion Injury in a Rat Model.

Wu, Di / Liu, Jingyu / Zhou, Changcheng / Ma, Wenjie / Zhou, Liuhua / Ge, Yuzheng / Jia, Ruipeng

Bioengineering (Basel, Switzerland)

2023 Volume 10, Issue 5

Abstract: Renal ischemia-reperfusion injury (IRI) is a significant cause of acute kidney injury (AKI) and usually brings severe public health consequences. Adipose-derived endothelial progenitor cell (AdEPCs) transplantation is beneficial for AKI but suffers from ... ...

Abstract	Renal ischemia-reperfusion injury (IRI) is a significant cause of acute kidney injury (AKI) and usually brings severe public health consequences. Adipose-derived endothelial progenitor cell (AdEPCs) transplantation is beneficial for AKI but suffers from low delivery efficiency. This study was conducted to explore the protective effects of magnetically delivered AdEPCs on the repair of renal IRI. Two types of magnetic delivery methods, namely the endocytosis magnetization (EM) method and the immunomagnetic (IM) method were fabricated using PEG@Fe
Language	English
Publishing date	2023-04-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2746191-9
ISSN	2306-5354
ISSN	2306-5354
DOI	10.3390/bioengineering10050509
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Article: Dynamic regulation of anti-oxidation following donation repairing after circulatory determined death renal transplantation with prolonged non-heart-beating time.

Wang, Xinning / Zhou, Changcheng / Liu, Jingyu / Jia, Ruipeng

Journal of biomedical research

2021 Volume 35, Issue 5, Page(s) 383–394

Abstract: Donation after circulatory-determined death (DCD) is an important part of renal transplantation. Therefore, DCD renal transplantation animal model should be established to study the mechanism of organ injury. Here, we established a stable DCD rat renal ... ...

Abstract	Donation after circulatory-determined death (DCD) is an important part of renal transplantation. Therefore, DCD renal transplantation animal model should be established to study the mechanism of organ injury. Here, we established a stable DCD rat renal transplantation model and investigated the dynamic regulation of graft self-repairing and antioxidant capacities with different non-heart-beating times (NHBTs). Male Sprague-Dawley rats were randomly divided into four groups with the NHBT of the donors from 0 to 15, 30, and 45 minutes. Recipients in long NHBT groups had a significantly lower survival rate and poorer graft function than those in short NHBT groups. Grafts from the 15-minute and 30-minute NHBT groups showed light and severe injury respectively at an early stage after transplantation and recovered within 7 days after transplantation, whereas the self-repairing of the grafts in the 45-minute NHBT group was delayed. The expressions of proliferating cell nuclear antigen (PCNA) and von Willebrand factor (vWF) were dependent on NHBT. The expression of antioxidant proteins paralleled graft recovery. In conclusion, the recipients can up-regulate antioxidant capacity to enhance graft self-repairing in DCD renal transplantation. Prolonged NHBT can delay the self-repairing and antioxidation of grafts.
Language	English
Publishing date	2021-10-07
Publishing country	China
Document type	Journal Article
ZDB-ID	2555537-6
ISSN	1876-4819 ; 1674-8301
ISSN (online)	1876-4819
ISSN	1674-8301
DOI	10.7555/JBR.35.20210031
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Article ; Online: Fibroblast-specific IKK-β deficiency ameliorates angiotensin II-induced adverse cardiac remodeling in mice.

Lu, Weiwei / Meng, Zhaojie / Hernandez, Rebecca / Zhou, Changcheng

JCI insight

2021 Volume 6, Issue 18

Abstract: Cardiac inflammation and fibrosis contribute significantly to hypertension-related adverse cardiac remodeling. IκB kinase β (IKK-β), a central coordinator of inflammation through activation of NF-κB, has been demonstrated as a key molecular link between ... ...

Abstract	Cardiac inflammation and fibrosis contribute significantly to hypertension-related adverse cardiac remodeling. IκB kinase β (IKK-β), a central coordinator of inflammation through activation of NF-κB, has been demonstrated as a key molecular link between inflammation and cardiovascular disease. However, the cell-specific contribution of IKK-β signaling toward adverse cardiac remodeling remains elusive. Cardiac fibroblasts are one of the most populous nonmyocyte cell types in the heart that play a key role in mediating cardiac fibrosis and remodeling. To investigate the function of fibroblast IKK-β, we generated inducible fibroblast-specific IKK-β-deficient mice. Here, we report an important role of IKK-β in the regulation of fibroblast functions and cardiac remodeling. Fibroblast-specific IKK-β-deficient male mice were protected from angiotensin II-induced cardiac hypertrophy, fibrosis, and macrophage infiltration. Ablation of fibroblast IKK-β inhibited angiotensin II-stimulated fibroblast proinflammatory and profibrogenic responses, leading to ameliorated cardiac remodeling and improved cardiac function in IKK-β-deficient mice. Findings from this study establish fibroblast IKK-β as a key factor regulating cardiac fibrosis and function in hypertension-related cardiac remodeling.
MeSH term(s)	Angiotensin II/pharmacology ; Animals ; Blood Pressure/drug effects ; Cardiomegaly/chemically induced ; Cardiomegaly/genetics ; Cardiomegaly/pathology ; Cardiomegaly/physiopathology ; Cell Differentiation/drug effects ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Collagen Type I/metabolism ; Fibroblasts/physiology ; Fibrosis ; Gene Knockdown Techniques ; Heart Rate/drug effects ; Hypertension/chemically induced ; I-kappa B Kinase/genetics ; Inflammation/metabolism ; Macrophages ; Male ; Mice ; Myocarditis/genetics ; Myocarditis/metabolism ; Myocardium/pathology ; Organ Size ; Protective Factors ; Signal Transduction ; Ventricular Remodeling/genetics
Chemical Substances	Collagen Type I ; Angiotensin II (11128-99-7) ; I-kappa B Kinase (EC 2.7.11.10) ; Ikbkb protein, mouse (EC 2.7.11.10)
Language	English
Publishing date	2021-09-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.150161
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Article: Long Noncoding RNA LINC00467: Role in Various Human Cancers.

Wu, Di / Li, Rongfei / Liu, Jingyu / Zhou, Changcheng / Jia, Ruipeng

Frontiers in genetics

2022 Volume 13, Page(s) 892009

Abstract: Intricate genetic mutations promote the progression of different cancer types. Long noncoding RNAs (lncRNAs) have been widely demonstrated to participate in the genomic activities of various human cancers. Long intergenic non-coding RNA 467 (LINC00467) ... ...

Abstract	Intricate genetic mutations promote the progression of different cancer types. Long noncoding RNAs (lncRNAs) have been widely demonstrated to participate in the genomic activities of various human cancers. Long intergenic non-coding RNA 467 (LINC00467) is an upregulated lncRNA in diverse diseases, especially in several types of cancers. Functional experiments of LINC00467 revealed that LINC00467 overexpression enhanced cell chemoresistance, proliferation, migration, and invasion in several types of cancers. Moreover, overexpressed LINC00467 was associated with a poor clinical prognosis. The present evidence suggests that LINC00467 may serve as a promising prognostic indicator and become a novel cancer therapeutic target. In this review, we introduce the biologic functions of lncRNAs and describe the molecular mechanism and clinical significance of LINC00467 in detail.
Language	English
Publishing date	2022-06-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2022.892009
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Article ; Online: Platelet-derived thrombospondin 1 promotes immune cell liver infiltration and exacerbates diet-induced steatohepatitis.

Gwag, Taesik / Lee, Sangderk / Li, Zhenyu / Newcomb, Alana / Otuagomah, Josephine / Weinman, Steven A / Liang, Ying / Zhou, Changcheng / Wang, Shuxia

JHEP reports : innovation in hepatology

2024 Volume 6, Issue 4, Page(s) 101019

Abstract: Background & aims: Recent studies have implicated platelets, particularly α-granules, in the development of non-alcoholic steatohepatitis (NASH). However, the specific mechanisms involved have yet to be determined. Notably, thrombospondin 1 (TSP1) is a ... ...

Abstract	Background & aims: Recent studies have implicated platelets, particularly α-granules, in the development of non-alcoholic steatohepatitis (NASH). However, the specific mechanisms involved have yet to be determined. Notably, thrombospondin 1 (TSP1) is a major component of the platelet α-granules released during platelet activation. Hence, we aimed to determine the role of platelet-derived TSP1 in NASH. Methods: Platelet-specific Results: Although TSP1 deletion in platelets did not affect diet-induced steatosis, Conclusions: These data suggest that platelet α-granule-derived TSP1 is a significant contributor to diet-induced NASH and fibrosis, potentially serving as a new therapeutic target for this severe liver disease. Impact and implications: Recent studies have implicated platelets, specifically α-granules, in the development of non-alcoholic steatohepatitis, yet the precise mechanisms remain unknown. In this study, through the utilization of a tissue-specific knockout mouse model and human 3D liver organoid, we demonstrated that platelet α-granule-derived TSP1 significantly contributes to diet-induced non-alcoholic steatohepatitis and fibrosis. This contribution is, in part, attributed to the regulation of intrahepatic immune cell infiltration and potential crosstalk between fat and the liver. These findings suggest that platelet-derived TSP1 may represent a novel therapeutic target in non-alcoholic fatty liver disease.
Language	English
Publishing date	2024-01-26
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2024.101019
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Article ; Online: Neutrophil-derived nanovesicles deliver IL-37 to mitigate renal ischemia-reperfusion injury via endothelial cell targeting.

Ma, Wenjie / Wu, Di / Long, Chengcheng / Liu, Jingyu / Xu, Luwei / Zhou, Liuhua / Dou, Quanliang / Ge, Yuzheng / Zhou, Changcheng / Jia, Ruipeng

Journal of controlled release : official journal of the Controlled Release Society

2024 Volume 370, Page(s) 66–81

Abstract: Renal ischemia-reperfusion injury (IRI) is one of the most important causes of acute kidney injury (AKI). Interleukin (IL)-37 has been suggested as a novel anti-inflammatory factor for the treatment of IRI, but its application is still limited by its low ...

Abstract	Renal ischemia-reperfusion injury (IRI) is one of the most important causes of acute kidney injury (AKI). Interleukin (IL)-37 has been suggested as a novel anti-inflammatory factor for the treatment of IRI, but its application is still limited by its low stability and delivery efficiency. In this study, we reported a novel engineered method to efficiently and easily prepare neutrophil membrane-derived vesicles (N-MVs), which could be utilized as a promising vehicle to deliver IL-37 and avoid the potential side effects of neutrophil-derived natural extracellular vesicles. N-MVs could enhance the stability of IL-37 and targetedly deliver IL-37 to damaged endothelial cells of IRI kidneys via P-selectin glycoprotein ligand-1 (PSGL-1). In vitro and in vivo evidence revealed that N-MVs encapsulated with IL-37 (N-MV@IL-37) could inhibit endothelial cell apoptosis, promote endothelial cell proliferation and angiogenesis, and decrease inflammatory factor production and leukocyte infiltration, thereby ameliorating renal IRI. Our study establishes a promising delivery vehicle for the treatment of renal IRI and other endothelial damage-related diseases.
Language	English
Publishing date	2024-04-17
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	632533-6
ISSN	1873-4995 ; 0168-3659
ISSN (online)	1873-4995
ISSN	0168-3659
DOI	10.1016/j.jconrel.2024.04.025
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