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CCR5 deletion impairs the post‐myocardial infarction inflammatory response
Author(s) -
Zamilpa Rogelio,
Cigarroa Joaquin,
Dai Qiuxia,
Escobar G. Patricia,
Jimenez Fabio,
Martinez Hernan G.,
Ahuja Seema S.,
Lindsey Merry L.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.362.3
Subject(s) - myocardial infarction , chemokine , ventricle , wound healing , inflammation , medicine , ccl3 , receptor , neovascularization
The inflammatory response following a myocardial infarction (MI) regulates multiple components of the wound healing process. In particular, macrophages regulate wound debridement, scar formation, and neovascularization. The CC Chemokine Receptor 5 (CCR5) is a key chemokine receptor expressed on macrophages, and CCR5 ligands are highly upregulated post‐MI. However, the roles of CCR5 post‐MI have not been investigated. Accordingly, we examined macrophage infiltration and collagen concentration in the left ventricle (LV) and plasma inflammatory markers in wild‐type mice (wt, n=25) and CCR5 null mice (null, n=33). The groups had similar infarct sizes (44±2% in wt and 42±2% in null, p= n.s.). Macrophage infiltration was lower in the null (7±1% of total infarct area compared to 11±1% in wt; p<0.05). The collagen insoluble to soluble ratio was 36.7% higher in the null (p<0.05), suggesting reduced collagen synthesis. In addition, plasma levels of IL‐6, IFN‐ ? and TNFá increased in wt, but not in null mice, post‐MI (p<0.05). We conclude that CCR5 deletion has a net negative effect on remodeling post‐MI, as evidenced by a decreased inflammatory response and collagen synthesis. NIH (R01 HL‐75360) and American Heart Association grant (0855119F) to M.L.L. and T32 (HL07446) to R.Z.