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month download article/chapter christoph bode & sebastian grundmann neutrophil-induced ischemia-reperfusion injury ischemia/reperfusion-induced cardiac injury ischemia/reperfusion-induced leukocyte adhesion lipopolysaccharide/tnf-alpha stimulation hepatic ischemia-reperfusion injury real-time digital imaging article basic research ir-related tissue injury myeloid-derived suppressor cells apolipoprotein e-deficient mice leukocyte-endothelial cell interaction respiratory oxidative burst full article pdf quantifying microrna-expression levels acute myocardial infarction anti-inflammatory strategy microrna-155 targets socs1 ischemia–reperfusion injury ischemia-reperfusion injury major causal factor inflammatory autoimmune diseases myocardial reperfusion injury human muscle tissue upregulates tnf-alpha privacy choices/manage cookies interleukin-1 signaling pathway hausenloy dj murine myocardial infarction myocardial infarction reveals reperfusion injury resulted coronary artery disease receptor 4-deficient mice decreased macrophage inflammation pathological cardiac hypertrophy free muscle flaps reactive oxygen species measuring reactive oxygen microrna-155 promotes atherosclerosis inflammatory cell recruitment rat cremaster muscle microrna-155 deficiency results hematopoietic stem cells article eisenhardt leukocyte-endothelial interaction related subjects regulatory protein cd47 collagen fiber deposition interleukin-1 receptor antagonist

Questions {❓}

• Rashid MA, William-Olsson G (1991) Are leukocytosis and lipid peroxidation involved in ischemic or reperfusion injury in cardiac surgery?

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         headline:MicroRNA-155 aggravates ischemia–reperfusion injury by modulation of inflammatory cell recruitment and the respiratory oxidative burst
         description:The inflammatory sequelae of ischemia–reperfusion injury (IRI) are a major causal factor of tissue injury in various clinical settings. MicroRNAs (miRs) are short, non-coding RNAs, which regulate protein expression. Here, we investigated the role of miR-155 in IR-related tissue injury. Quantifying microRNA-expression levels in a human muscle tissue after IRI, we found miR-155 expression to be significantly increased and to correlate with the increased expression of TNF-α, IL-1β, CD105, and Caspase3 as well as with leukocyte infiltration. The direct miR-155 target gene SOCS-1 was downregulated. In a mouse model of myocardial infarction, temporary LAD ligation and reperfusion injury resulted in a smaller area of necrosis in miR-155−/− animals compared to wildtype animals. To investigate the underlying mechanisms, we evaluated the effect of miR-155 on inflammatory cell recruitment by intravital microscopy and on the generation of reactive oxygen species (ROS) of macrophages. Our intravital imaging results demonstrated a decreased recruitment of inflammatory cells in miR-155−/− animals during IRI. The generation of ROS in leukocytic cells of miR-155−/− animals was also reduced. RNA silencing of the direct miR-155 target gene SOCS-1 abrogated this effect. In conclusion, miR-155 aggravates the inflammatory response, leukocyte infiltration and tissue damage in IRI via modulation of SOCS-1-dependent generation of ROS. MiR-155 is thus a potential target for the treatment or prevention of IRI.
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      headline:MicroRNA-155 aggravates ischemia–reperfusion injury by modulation of inflammatory cell recruitment and the respiratory oxidative burst
      description:The inflammatory sequelae of ischemia–reperfusion injury (IRI) are a major causal factor of tissue injury in various clinical settings. MicroRNAs (miRs) are short, non-coding RNAs, which regulate protein expression. Here, we investigated the role of miR-155 in IR-related tissue injury. Quantifying microRNA-expression levels in a human muscle tissue after IRI, we found miR-155 expression to be significantly increased and to correlate with the increased expression of TNF-α, IL-1β, CD105, and Caspase3 as well as with leukocyte infiltration. The direct miR-155 target gene SOCS-1 was downregulated. In a mouse model of myocardial infarction, temporary LAD ligation and reperfusion injury resulted in a smaller area of necrosis in miR-155−/− animals compared to wildtype animals. To investigate the underlying mechanisms, we evaluated the effect of miR-155 on inflammatory cell recruitment by intravital microscopy and on the generation of reactive oxygen species (ROS) of macrophages. Our intravital imaging results demonstrated a decreased recruitment of inflammatory cells in miR-155−/− animals during IRI. The generation of ROS in leukocytic cells of miR-155−/− animals was also reduced. RNA silencing of the direct miR-155 target gene SOCS-1 abrogated this effect. In conclusion, miR-155 aggravates the inflammatory response, leukocyte infiltration and tissue damage in IRI via modulation of SOCS-1-dependent generation of ROS. MiR-155 is thus a potential target for the treatment or prevention of IRI.
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