1. Ccr1 deficiency reduces inflammatory remodelling and preserves left ventricular function after myocardial infarction
- Author
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Yassin Djalali-Talab, Marc W. Merx, Christian Weber, S Becher, Otilia Postea, Elisa A. Liehn, Malte Kelm, Erdenechimeg Shagdarsuren, and Alma Zernecke
- Subjects
medicine.medical_specialty ,medicine.medical_treatment ,Population ,Myocardial Infarction ,Receptors, CCR1 ,Inflammation ,Blood Pressure ,Ventricular Function, Left ,Mice ,Internal medicine ,medicine ,Animals ,myocardial remodelling ,Platelet activation ,Myocardial infarction ,education ,Mice, Knockout ,education.field_of_study ,business.industry ,chemokine receptor ,leukocyte recruitment ,Cell Biology ,Articles ,medicine.disease ,Coronary Vessels ,Mice, Inbred C57BL ,Disease Models, Animal ,Cytokine ,medicine.anatomical_structure ,Ventricle ,Regional Blood Flow ,Cardiology ,Molecular Medicine ,medicine.symptom ,Ligation ,business ,Myofibroblast - Abstract
Myocardial necrosis triggers inflammatory changes and a complex cytokine cascade that are only incompletely understood. The chemokine receptor CCR1 mediates inflammatory recruitment in response to several ligands released by activated platelets and up-regulated after myocardial infarction (MI). Here, we assess the effect of CCR1 on remodelling after MI using Ccr1-deficient (Ccr1(-)(/-)) mice. MI was induced in Ccr1(-/-) or wild-type mice by proximal ligation of the left anterior descending (LAD). Mice were sacrificed and analysed at day 1, 4, 7, 14 and 21 after MI. While initial infarct areas and areas at risk did not differ between groups, infarct size increased to 20.6+/-8.4% of the left ventricle (LV) in wild-type mice by day 21 but remained at 11.2+/-1.2% of LV (P
- Published
- 2007