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• W2288940062 abstract "BackgroundSuppressor of cytokine signaling-3 (SOCS3) is a cytokine-inducible negative regulator of JAK-STAT signaling pathway. We previously showed that cardiac-specific SOCS3 knockout mice (SOCS3-CKO) are resistant to myocardial ischemia reperfusion injury (IRI). In the present study, we sought to identify the effect of cardiac-specific SOCS3 deletion on gene expression using DNA microarray analysis.Methods and ResultsWild-type (WT) and SOCS3-CKO mice were subjected to myocardial IRI. The infarct size 24 h after reperfusion was significantly reduced and cardiac function was preserved in SOCS3-CKO mice compared with WT mice. We divided mice into four groups, including controls with a sham operation, WT with an IRI, SOCS3-CKO with a sham operation, and SOCS3CKO with an IRI (n=5, in each group). DNA microarray analysis was conducted using the hearts from mice 3 h after IRI. Pathway analysis on the genes that respond differentially to IRI in SOCS3CKO than in WT mice highlights genes involved in cell cycle, cytokine and inflammatory response pathway, and response to external stimuli and wounding. These genes included interleukin-1 (IL1), IL-6, TNFalpha, Nfkb2, Relb, CCL and CXCL chemokines. In situ hybridaization revealed that G-CSF is expressed on infiltrated leukocytes within myocardium after reperfusion.ConclusionThese results suggested that myocardial IR injury may have been prevented in SOCS3-CKO by inhibition of the pro-inflammatory pathways and response to external stimuli. BackgroundSuppressor of cytokine signaling-3 (SOCS3) is a cytokine-inducible negative regulator of JAK-STAT signaling pathway. We previously showed that cardiac-specific SOCS3 knockout mice (SOCS3-CKO) are resistant to myocardial ischemia reperfusion injury (IRI). In the present study, we sought to identify the effect of cardiac-specific SOCS3 deletion on gene expression using DNA microarray analysis. Suppressor of cytokine signaling-3 (SOCS3) is a cytokine-inducible negative regulator of JAK-STAT signaling pathway. We previously showed that cardiac-specific SOCS3 knockout mice (SOCS3-CKO) are resistant to myocardial ischemia reperfusion injury (IRI). In the present study, we sought to identify the effect of cardiac-specific SOCS3 deletion on gene expression using DNA microarray analysis. Methods and ResultsWild-type (WT) and SOCS3-CKO mice were subjected to myocardial IRI. The infarct size 24 h after reperfusion was significantly reduced and cardiac function was preserved in SOCS3-CKO mice compared with WT mice. We divided mice into four groups, including controls with a sham operation, WT with an IRI, SOCS3-CKO with a sham operation, and SOCS3CKO with an IRI (n=5, in each group). DNA microarray analysis was conducted using the hearts from mice 3 h after IRI. Pathway analysis on the genes that respond differentially to IRI in SOCS3CKO than in WT mice highlights genes involved in cell cycle, cytokine and inflammatory response pathway, and response to external stimuli and wounding. These genes included interleukin-1 (IL1), IL-6, TNFalpha, Nfkb2, Relb, CCL and CXCL chemokines. In situ hybridaization revealed that G-CSF is expressed on infiltrated leukocytes within myocardium after reperfusion. Wild-type (WT) and SOCS3-CKO mice were subjected to myocardial IRI. The infarct size 24 h after reperfusion was significantly reduced and cardiac function was preserved in SOCS3-CKO mice compared with WT mice. We divided mice into four groups, including controls with a sham operation, WT with an IRI, SOCS3-CKO with a sham operation, and SOCS3CKO with an IRI (n=5, in each group). DNA microarray analysis was conducted using the hearts from mice 3 h after IRI. Pathway analysis on the genes that respond differentially to IRI in SOCS3CKO than in WT mice highlights genes involved in cell cycle, cytokine and inflammatory response pathway, and response to external stimuli and wounding. These genes included interleukin-1 (IL1), IL-6, TNFalpha, Nfkb2, Relb, CCL and CXCL chemokines. In situ hybridaization revealed that G-CSF is expressed on infiltrated leukocytes within myocardium after reperfusion. ConclusionThese results suggested that myocardial IR injury may have been prevented in SOCS3-CKO by inhibition of the pro-inflammatory pathways and response to external stimuli. These results suggested that myocardial IR injury may have been prevented in SOCS3-CKO by inhibition of the pro-inflammatory pathways and response to external stimuli." @default.
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• W2288940062 date "2015-10-01" @default.
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• W2288940062 title "Change of Transcriptional Profile in Response to Cardiac-Specific Deletion of SOCS3 after Myocardial Ischemia Reperfusion Injury" @default.
• W2288940062 doi "https://doi.org/10.1016/j.cardfail.2015.08.186" @default.
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