β‐catenin regulates innate and adaptive immunity in mouse liver ischemia‐reperfusion injury
Dendritic cells (DCs) are critical mediators of immune responses that integrate signals from the innate immune system to orchestrate adaptive host immunity. This study was designed to investigate the role and molecular mechanisms of STAT3‐induced β‐catenin in the regulation of DC function and inflam...
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Published in | Hepatology (Baltimore, Md.) Vol. 57; no. 3; pp. 1203 - 1214 |
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Language | English |
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Abstract | Dendritic cells (DCs) are critical mediators of immune responses that integrate signals from the innate immune system to orchestrate adaptive host immunity. This study was designed to investigate the role and molecular mechanisms of STAT3‐induced β‐catenin in the regulation of DC function and inflammatory responses in vitro and in vivo. STAT3 induction in lipopolysaccharide (LPS)‐stimulated mouse bone marrow‐derived DCs (BMDCs) triggered β‐catenin activation by way of GSK‐3β phosphorylation. The activation of β‐catenin inhibited phosphatase and tensin homolog delete on chromosome 10 (PTEN) and promoted the phosphoinositide 3‐kinase (PI3K)/Akt pathway, which in turn down‐regulated DC maturation and function. In contrast, knockdown of β‐catenin increased PTEN/TLR4 (Toll‐like receptor 4), interferon regulatory factor‐3 (IRF3), nuclear factor kappa B (NF‐κB) activity, and proinflammatory cytokine programs in response to LPS stimulation. In a mouse model of warm liver ischemia and reperfusion injury (IRI), disruption of β‐catenin signaling increased the hepatocellular damage, enhanced hepatic DC maturation/function, and PTEN/TLR4 local inflammation in vivo. Conclusion: These findings underscore the role of β‐catenin to modulate DC maturation and function at the innate‐adaptive interface. Activation of β‐catenin triggered PI3K/Akt, which in turn inhibited TLR4‐driven inflammatory response in a negative feedback regulatory mechanism. By identifying the molecular pathways by which β‐catenin regulates DC function, our findings provide the rationale for novel therapeutic approaches to manage local inflammation and injury in IR‐stressed liver. (HEPATOLOGY 2013) |
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AbstractList | Dendritic cells (DCs) are critical mediators of immune responses that integrate signals from the innate immune system to orchestrate adaptive host immunity. This study was designed to investigate the role and molecular mechanisms of STAT3‐induced β‐catenin in the regulation of DC function and inflammatory responses in vitro and in vivo. STAT3 induction in lipopolysaccharide (LPS)‐stimulated mouse bone marrow‐derived DCs (BMDCs) triggered β‐catenin activation by way of GSK‐3β phosphorylation. The activation of β‐catenin inhibited phosphatase and tensin homolog delete on chromosome 10 (PTEN) and promoted the phosphoinositide 3‐kinase (PI3K)/Akt pathway, which in turn down‐regulated DC maturation and function. In contrast, knockdown of β‐catenin increased PTEN/TLR4 (Toll‐like receptor 4), interferon regulatory factor‐3 (IRF3), nuclear factor kappa B (NF‐κB) activity, and proinflammatory cytokine programs in response to LPS stimulation. In a mouse model of warm liver ischemia and reperfusion injury (IRI), disruption of β‐catenin signaling increased the hepatocellular damage, enhanced hepatic DC maturation/function, and PTEN/TLR4 local inflammation in vivo. Conclusion: These findings underscore the role of β‐catenin to modulate DC maturation and function at the innate‐adaptive interface. Activation of β‐catenin triggered PI3K/Akt, which in turn inhibited TLR4‐driven inflammatory response in a negative feedback regulatory mechanism. By identifying the molecular pathways by which β‐catenin regulates DC function, our findings provide the rationale for novel therapeutic approaches to manage local inflammation and injury in IR‐stressed liver. (HEPATOLOGY 2013) UNLABELLEDDendritic cells (DCs) are critical mediators of immune responses that integrate signals from the innate immune system to orchestrate adaptive host immunity. This study was designed to investigate the role and molecular mechanisms of STAT3-induced β-catenin in the regulation of DC function and inflammatory responses in vitro and in vivo. STAT3 induction in lipopolysaccharide (LPS)-stimulated mouse bone marrow-derived DCs (BMDCs) triggered β-catenin activation by way of GSK-3β phosphorylation. The activation of β-catenin inhibited phosphatase and tensin homolog delete on chromosome 10 (PTEN) and promoted the phosphoinositide 3-kinase (PI3K)/Akt pathway, which in turn down-regulated DC maturation and function. In contrast, knockdown of β-catenin increased PTEN/TLR4 (Toll-like receptor 4), interferon regulatory factor-3 (IRF3), nuclear factor kappa B (NF-κB) activity, and proinflammatory cytokine programs in response to LPS stimulation. In a mouse model of warm liver ischemia and reperfusion injury (IRI), disruption of β-catenin signaling increased the hepatocellular damage, enhanced hepatic DC maturation/function, and PTEN/TLR4 local inflammation in vivo. CONCLUSIONThese findings underscore the role of β-catenin to modulate DC maturation and function at the innate-adaptive interface. Activation of β-catenin triggered PI3K/Akt, which in turn inhibited TLR4-driven inflammatory response in a negative feedback regulatory mechanism. By identifying the molecular pathways by which β-catenin regulates DC function, our findings provide the rationale for novel therapeutic approaches to manage local inflammation and injury in IR-stressed liver. Dendritic cells (DCs) are critical mediators of immune responses that integrate signals from the innate immune system to orchestrate adaptive host immunity. This study was designed to investigate the role and molecular mechanisms of STAT3-induced β-catenin in the regulation of DC function and inflammatory responses in vitro and in vivo. STAT3 induction in LPS-stimulated mouse bone marrow derived-DCs (BMDCs) triggered β-catenin activation via GSK-3β phosphorylation. The activation of β-catenin inhibited PTEN and promoted PI3K/Akt pathway, which in turn dowregulated DC maturation and function. In contrast, knockdown of β-catenin increased PTEN/TLR4, IRF3, NF-κB activity and proinflammatory cytokine programs in response to LPS stimulation. In a mouse model of warm liver ischemia and reperfusion injury (IRI), disruption of β-catenin signaling increased the hepatocellular damage, enhanced hepatic DC maturation/function and PTEN/TLR4 local inflammation in vivo . Conclusion: Our novel findings underscore the role of β-catenin to modulate DC maturation and function at the innate - adaptive interface. Activation of β-catenin triggered PI3K/Akt which in turn inhibited TLR4-driven inflammatory response in a negative feedback regulatory mechanism. By identifying the molecular pathways by which β-catenin regulates DC function, our findings provide the rationale for novel therapeutic approaches to manage local inflammation and injury in IR-stressed liver. Dendritic cells (DCs) are critical mediators of immune responses that integrate signals from the innate immune system to orchestrate adaptive host immunity. This study was designed to investigate the role and molecular mechanisms of STAT3-induced β-catenin in the regulation of DC function and inflammatory responses in vitro and in vivo. STAT3 induction in lipopolysaccharide (LPS)-stimulated mouse bone marrow-derived DCs (BMDCs) triggered β-catenin activation by way of GSK-3β phosphorylation. The activation of β-catenin inhibited phosphatase and tensin homolog delete on chromosome 10 (PTEN) and promoted the phosphoinositide 3-kinase (PI3K)/Akt pathway, which in turn down-regulated DC maturation and function. In contrast, knockdown of β-catenin increased PTEN/TLR4 (Toll-like receptor 4), interferon regulatory factor-3 (IRF3), nuclear factor kappa B (NF-κB) activity, and proinflammatory cytokine programs in response to LPS stimulation. In a mouse model of warm liver ischemia and reperfusion injury (IRI), disruption of β-catenin signaling increased the hepatocellular damage, enhanced hepatic DC maturation/function, and PTEN/TLR4 local inflammation in vivo. These findings underscore the role of β-catenin to modulate DC maturation and function at the innate-adaptive interface. Activation of β-catenin triggered PI3K/Akt, which in turn inhibited TLR4-driven inflammatory response in a negative feedback regulatory mechanism. By identifying the molecular pathways by which β-catenin regulates DC function, our findings provide the rationale for novel therapeutic approaches to manage local inflammation and injury in IR-stressed liver. |
Author | Yue, Shi Kamo, Naoko Shen, Xiu‐Da Ke, Bibo Busuttil, Ronald W. Gao, Feng Kupiec‐Weglinski, Jerzy W. Ji, Haofeng |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23081841$$D View this record in MEDLINE/PubMed |
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SubjectTerms | Adaptive Immunity - physiology Animals Apoptosis - immunology beta Catenin - genetics beta Catenin - immunology beta Catenin - metabolism Cells, Cultured Dendritic Cells - cytology Dendritic Cells - immunology Dendritic Cells - metabolism Disease Models, Animal Immunity, Innate - physiology Liver Diseases - immunology Liver Diseases - metabolism Male Mice Mice, Inbred C57BL PTEN Phosphohydrolase - immunology PTEN Phosphohydrolase - metabolism Reperfusion Injury - immunology Reperfusion Injury - metabolism RNA, Small Interfering - genetics Signal Transduction - immunology STAT3 Transcription Factor - immunology STAT3 Transcription Factor - metabolism Toll-Like Receptor 4 - immunology Toll-Like Receptor 4 - metabolism |
Title | β‐catenin regulates innate and adaptive immunity in mouse liver ischemia‐reperfusion injury |
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