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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Strecker, Jan-Kolja Schilling, Matthias Schäbitz, Wolf-Rüdiger Gess, Burkhard Minnerup, Jens Schütte-Nütgen, Katharina |
| Description | Country affiliation: Germany Author Affiliation: Strecker JK ( Department of Neurology, University of Münster, Albert-Schweitzer Campus A1, Münster, Germany. strecker.jan@gmx.de) |
| Abstract | BACKGROUND AND PURPOSE: Stroke-induced blood-brain barrier (BBB)-disruption can contribute to further progression of cerebral damage. There is rising evidence for a strong involvement of chemokines in postischemic BBB-breakdown. In a previous study, we showed that monocyte chemoattractant protein-1 (MCP-1)-deficiency results in a markedly reduced inflammatory reaction with decreased levels of interleukin-6, interleukin-1ß, and granulocyte colony-stimulating factor after experimental stroke. With MCP-1 as one of the key players in stroke-induced inflammation, in this study, we investigated the influence of MCP-1 on poststroke BBB-disruption as well as transcription/translation of BBB-related genes/proteins after cerebral ischemia. METHODS: Sixteen wild-type and 16 MCP-1(-/-) mice were subjected to 30 minutes of middle cerebral artery occlusion. By injecting high molecular-tracer, we compared the degree of BBB-disruption after middle cerebral artery occlusion. Real-time polymerase chain reactions and Western blot technique were used to compare tight-junction gene expression, protein secretion, and BBB-leakage. RESULTS: Here, we report that MCP-1-deficiency results in a reduced BBB-leakage and a diminished expression of BBB-related genes occludin, zonula occludens-1, and zonula occludens-2. Real-time polymerase chain reactions and Western blot analysis revealed elevated claudin-5-levels in MCP-1(-/-) animals. MCP-1-deficiency resulted in reduced infarct sizes and an increased vascular accumulation of fluorescein-isothiocyanate-albumin. CONCLUSIONS: The results of the study provide further insights into the molecular mechanisms of BBB-opening and may help to better understand the mechanisms of infarct development after cerebral ischemia. |
| ISSN | 00392499 |
| e-ISSN | 15244628 |
| Journal | Stroke |
| Issue Number | 9 |
| Volume Number | 44 |
| Language | English |
| Publisher | Lippincott Williams & Wilkins (on behalf of the American Heart Association) |
| Publisher Date | 2013-09-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Blood-brain Barrier Metabolism Chemokine Ccl2 Deficiency Genetics Infarction, Middle Cerebral Artery Animals Pathology Physiopathology Disease Models, Animal Gene Expression Regulation Etiology Inflammation Immunology Mice Mice, Inbred C57bl Mice, Knockout Protein Biosynthesis Research Support, Non-u.s. Gov't Discipline Cardiology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cardiology and Cardiovascular Medicine Neuroscience Advanced and Specialized Nursing Neurology (clinical) |
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