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2014 ; 32
(9
): 2502-15
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Complement component 3 is necessary to preserve myocardium and myocardial
function in chronic myocardial infarction
#MMPMID24806427
Wysoczynski M
; Solanki M
; Borkowska S
; van Hoose P
; Brittian KR
; Prabhu SD
; Ratajczak MZ
; Rokosh G
Stem Cells
2014[Sep]; 32
(9
): 2502-15
PMID24806427
show ga
Activation of the complement cascade (CC) with myocardial infarction (MI) acutely
initiates immune cell infiltration, membrane attack complex formation on injured
myocytes, and exacerbates myocardial injury. Recent studies implicate the CC in
mobilization of stem/progenitor cells and tissue regeneration. Its role in
chronic MI is unknown. Here, we consider complement component C3, in the chronic
response to MI. C3 knockout (KO) mice were studied after permanent coronary
artery ligation. C3 deficiency exacerbated myocardial dysfunction 28 days after
MI compared to WT with further impaired systolic function and LV dilation despite
similar infarct size 24 hours post-MI. Morphometric analysis 28 days post-MI
showed C3 KO mice had more scar tissue with less viable myocardium within the
infarct zone which correlated with decreased c-kit(pos) cardiac stem/progenitor
cells (CPSC), decreased proliferating Ki67(pos) CSPCs and decreased formation of
new BrdU(pos) /?-sarcomeric actin(pos) myocytes, and increased apoptosis compared
to WT. Decreased CSPCs and increased apoptosis were evident 7 days post-MI in C3
KO hearts. The inflammatory response with MI was attenuated in the C3 KO and was
accompanied by attenuated hematopoietic, pluripotent, and cardiac stem/progenitor
cell mobilization into the peripheral blood 72 hours post-MI. These results are
the first to demonstrate that CC, through C3, contributes to myocardial
preservation and regeneration in response to chronic MI. Responses in the C3 KO
infer that C3 activation in response to MI expands the resident CSPC population,
increases new myocyte formation, increases and preserves myocardium, inflammatory
response, and bone marrow stem/progenitor cell mobilization to preserve
myocardial function.
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