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2017 ; 7
(1
): 9999
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Resolution Agonist 15-epi-Lipoxin A(4) Programs Early Activation of Resolving
Phase in Post-Myocardial Infarction Healing
#MMPMID28855632
Kain V
; Liu F
; Kozlovskaya V
; Ingle KA
; Bolisetty S
; Agarwal A
; Khedkar S
; Prabhu SD
; Kharlampieva E
; Halade GV
Sci Rep
2017[Aug]; 7
(1
): 9999
PMID28855632
show ga
Following myocardial infarction (MI), overactive inflammation remodels the left
ventricle (LV) leading to heart failure coinciding with reduced levels of
15-epi-Lipoxin A(4) (15-epi LXA(4)). However, the role of 15-epi LXA(4) in
post-MI acute inflammatory response and resolving phase is unclear. We
hypothesize that liposomal fusion of 15-epi-LXA(4) (Lipo-15-epi-LXA(4)) or free
15-epi-LXA(4) will expedite the resolving phase in post-MI inflammation. 8 to
12-week-old male C57BL/6 mice were subjected to permanent coronary artery
ligation. Lipo-15-epi-LXA(4) or 15-epi-LXA(4) (1?µg/kg/day) was injected 3?hours
post-MI for (d)1 or continued daily till d5. 15-epi-LXA(4) activated formyl
peptide receptor (FPR2) and GPR120 on alternative macrophages but inhibited GPR40
on classical macrophages in-vitro. The 15-epi-LXA(4) injected mice displayed
reduced LV and lung mass to body weight ratios and improved ejection fraction at
d5 post-MI. In the acute phase of inflammation-(d1), 15-epi-LXA(4) primes
neutrophil infiltration with a robust increase of Ccl2 and FPR2 expression.
During the resolving phase-(d5), 15-epi-LXA(4) initiated rapid neutrophils
clearance with persistent activation of FPR2 in LV. Compared to MI-control,
15-epi-LXA(4) injected mice showed reduced renal inflammation along with
decreased levels of ngal and plasma creatinine. In summary, 15-epi-LXA(4)
initiates the resolving phase early to discontinue inflammation post-MI, thereby
reducing LV dysfunction.
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