AIMS: Dual therapy comprising @entity24778 for mobilization of bone marrow-derived progenitor cells (BMPCs), with simultaneous pharmacological inhibition of @entity33559 for enhanced myocardial recruitment of circulating BMPC via the SDF-1a/ @entity9843 -axis, has been shown to improve survival after @entity583 ( @entity583 ). Using an innovative method to provide non-invasive serial in vivo measurements and information on metabolic processes, we aimed to substantiate the possible effects of this therapeutic concept on @entity299 after @entity583 using @entity8983 positron emission tomography (FDG-PET). METHODS AND RESULTS: @entity583 was induced in C57BL/6 @entity19 by performing surgical ligation of the left anterior descending artery in these @entity19 . Animals were then treated with granulocyte-colony stimulating factor + @entity12350 ( @entity1412 ) or placebo for a duration of 5 days following @entity583 . From serial PET scans, we verified that the @entity1188 size in @entity1412 -treated @entity19 (n = 13) was significantly reduced at Day 30 after @entity583 when compared with the @entity19 receiving placebo (n = 10). Analyses showed a normalized FDG uptake on Day 6 in @entity1412 -treated @entity19 , indicating an attenuation of the cardiac inflammatory response to @entity583 in treated animals. Furthermore, flow cytometry showed a significant increase in the anti-inflammatory M2-macrophages subpopulation in @entity1412 -treated animals. In comparing @entity1412 treated with placebo animals, those receiving @entity1412 -therapy showed a reduction in @entity1283 and @entity5988 , which indicates the beneficial effect of @entity1412 treatment on @entity299 . Remarkably, flow cytometry and immunohistochemistry showed an increase of myocardial c-kit positive cells in treated @entity19 (n = 12 in both groups). CONCLUSION: Using the innovative method of micro-PET for non-invasive serial in vivo measurements of metabolic myocardial processes in @entity19 , we were able to provide mechanistic evidence that @entity1412 therapy improves cardiac regeneration and reduces adverse remodelling after @entity583 .

FDG-PET reveals improved cardiac regeneration and attenuated adverse remodelling following @entity12350 + @entity24778 therapy after XXXX .

@entity33559 :: ('13482(Tax:10090)', 'Gene') :: ['dipeptidylpeptidase-IV'] @entity5988 :: ('MESH:C565277', 'Disease') :: ['left ventricular dilatation'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity24778 :: ('12985(Tax:10090)', 'Gene') :: ['G-CSF'] @entity1283 :: ('MESH:D006332', 'Disease') :: ['myocardial hypertrophy'] @entity9843 :: ('12767(Tax:10090)', 'Gene') :: ['CXCR4'] @entity1188 :: ('MESH:D007238', 'Disease') :: ['infarct'] @entity12350 :: ('MESH:C496398', 'Chemical') :: ['Sitagliptin'] @entity299 :: ('MESH:D006331', 'Disease') :: ['cardiac remodelling'] @entity583 :: ('MESH:D009203', 'Disease') :: ['AMI', 'acute myocardial infarction'] @entity1412 :: ('MESH:D011125', 'Disease') :: ['GS'] @entity8983 :: ('CHEBI:49134', 'Chemical') :: ['2-deoxy-2-[18F]fluoro-d-glucose']
@entity583 :: (MESH:D009203,Disease) :: ['acute myocardial infarction']
