monocyte chemoattractant protein-1-deficiency impairs the expression of il-6, il-1β and g-csf after transient focal ischemia in mice单核细胞化学引诱物protein-1-deficiency损害il - 6的表达,il-1β瞬态小鼠局灶性缺血后,g - csf.pdfVIP

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2017-09-01 发布于上海
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monocyte chemoattractant protein-1-deficiency impairs the expression of il-6, il-1β and g-csf after transient focal ischemia in mice单核细胞化学引诱物protein-1-deficiency损害il - 6的表达,il-1β瞬态小鼠局灶性缺血后,g - csf.pdf

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monocyte chemoattractant protein-1-deficiency impairs the expression of il-6, il-1β and g-csf after transient focal ischemia in mice单核细胞化学引诱物protein-1-deficiency损害il - 6的表达,il-1β瞬态小鼠局灶性缺血后,g - csf

Monocyte Chemoattractant Protein-1-Deficiency Impairs the Expression of IL-6, IL-1b and G-CSF after Transient Focal Ischemia in Mice 1 . 1. 1 1 ¨ ¨ 1,2 Jan-Kolja Strecker * , Jens Minnerup , Burkhard Gess , E. Bernd Ringelstein , Wolf-Rudiger Schabitz , Matthias Schilling1 ¨ ¨ 1 Department of Neurology, University of Munster, Munster, Germany, 2 Department of Neurology, Evangelisches Krankenhaus, Bielefeld, Germany Abstract Monocyte chemoattractant protein-1 (MCP-1), a chemokine secreted by neurons and astrocytes following stroke is known to aggravate ischemia-related damage. Previous studies revealed that MCP-1-deficient mice develop smaller infarcts and have an improved neurological outcome, whereas mice overexpressing MCP-1 show worsened brain damage and impaired neurological function. The aim of the present study was to elucidate the molecular background of the enhanced recovery in MCP-1-deficient mice after stroke. For this purpose, we (1) performed expression analyses on crucial post-stroke related inflammatory genes in MCP-1-deficient mice compared to wildtype controls, (2) analyzed a possible impact of MCP-1 on astrocyte activation (3) investigated the cellular origin of respective inflammatory cytokines and (4) analyzed the impact of MCP-1 secretion on the migration of both neutrophil granulocytes and T-cells. Here we report that MCP-1-deficiency leads to a shift towards a less inflammatory state following experimental occlusion of the middle cerebral artery including an impaired induction of interleukin-6, interleukin-1b and granulocyte-colony stimulating factor expression