title: CXC chemokine KC fails to induce neutrophil infiltration and neoangiogenesis in a mouse model of myocardial infarction.
abstract: BACKGROUND
  Chemokines and neutrophils, known as important players in the inflammatory cascade, also contribute to heart tissue recovery and scar formation after myocardial infarction (MI). The objective of this study was to determine the importance of ELR-containing CXC chemokine KC in neutrophil infiltration and neoangiogenesis, in a mouse model of chronic MI.
  
  
  RESULTS
  MI was induced in mice divided in four groups: control (untreated), anti-KC "later" (anti-KC antibody injections started 4 days after MI and then delivered every 72 hours for 3 weeks, to inhibit angiogenesis), anti-KC "earlier" (anti-KC antibody injections 1 day before and 1 day after MI, to block neutrophil infiltration), anti-KC (anti-KC antibody injections 1 day before and 1 day after MI, and then every 72 hours for 3 weeks). The efficiency of the anti-KC treatment was determined by the measurement of KC serum concentration and immunofluorescence staining, in each of the four groups. Surprisingly, we did not find any difference in neutrophil infiltration in the infarcted area between untreated and treated animals. Moreover, the heart function, infarct size, and neoangiogenesis were not different between the four groups. As expected, a comparable anti-CXCR2 treatment of mice before and after MI was able to significantly reduce neutrophil infiltration into the infarcted area and angiogenesis, but also to reduce the infarction size after long or "later" treatment.
  
  
  CONCLUSIONS
  The major finding of our study is that KC, a potent neutrophil chemoattractant and an established angiogenic factor, failed to interfere in the post-infarction inflammatory response, in wound healing and scar formation after MI. Therefore, these aspects need to be carefully taken into account when devising therapeutic strategies for myocardial infarction and ischemic cardiomyopathy.
authors.affiliation: Institute for Molecular Cardiovascular Research, RWTH Aachen University, Aachen, Germany.
authors.forename: Hasan
authors.initials: H
authors.lastname: Oral
authors.forename: Isabella
authors.initials: I
authors.lastname: Kanzler
authors.forename: Nancy
authors.initials: N
authors.lastname: Tuchscheerer
authors.forename: Adelina
authors.initials: A
authors.lastname: Curaj
authors.forename: Sakine
authors.initials: S
authors.lastname: Simsekyilmaz
authors.forename: Tolga Taha
authors.initials: TT
authors.lastname: Sönmez
authors.forename: Eugen
authors.initials: E
authors.lastname: Radu
authors.forename: Otilia
authors.initials: O
authors.lastname: Postea
authors.forename: Christian
authors.initials: C
authors.lastname: Weber
authors.forename: Alexander
authors.initials: A
authors.lastname: Schuh
authors.forename: Elisa A
authors.initials: EA
authors.lastname: Liehn
mesh_terms: D043925:Angiogenesis Inducing Agents / Q000037:antagonists & inhibitors / Q000276:immunology* / Q000378:metabolism; D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D054360:Chemokine CXCL1 / Q000037:antagonists & inhibitors / Q000276:immunology* / Q000378:metabolism; D004195:Disease Models, Animal; D051379:Mice; D009203:Myocardial Infarction / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic / Q000187:drug effects / Q000276:immunology*; D020556:Neutrophil Infiltration / Q000187:drug effects / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors
chemical_list: D043925:Angiogenesis Inducing Agents; D000906:Antibodies; D054360:Chemokine CXCL1; C475895:Cxcl1 protein, mouse