Lack of IL-6 in knockout mice did not affect long-term mortality, myocardial infarction size, or left ventricular remodeling compared to wild-type controls at 6 weeks post-infarction.
Does IL-6 deficiency alter left ventricular remodeling, infarct size, and survival after experimental myocardial infarction in mice?
Endogenous IL-6 deficiency does not impact long-term infarct size, LV remodeling, or survival after myocardial infarction in mice, possibly due to compensatory mechanisms.
Circulating levels of interleukin (IL)-6 are elevated after myocardial infarction (MI) and associated with increased morbidity and mortality. Its myocardial expression post-MI suggests a pathophysiological role in this condition. To explore the role of endogenous IL-6, we analyzed MI size, left ventricular (LV) remodeling, and mortality after permanent coronary ligation in IL-6 knockout mice (IL-6-/-) and wild-type controls (WT). Six weeks after MI, IL-6-/- and WT had similar mortality rates, MI sizes, LV remodeling, and LV dysfunction in vivo, determined by catheterization. Infarct size 24 h post-MI, shown by 2,3,5-triphenyltetrazolium chloride (TTC) staining, was similar at 24 h. Treatment with exogenous IL-6 did not alter MI size in WT. Infarction resulted in marked phosphorylation of STAT3, without differences between genotypes. Leukemia inhibitory factor (LIF) protein was increased 48 h post-MI in IL-6-/-, and angiotensin II and AT1 receptor (AT1R) protein were strongly increased in IL-6-/- baseline and post-MI, suggesting compensatory up-regulation. Lack of IL-6 does not affect long-term MI size or LV function, remodeling, and survival. In mice lacking IL-6, other members of the IL-6 family such as LIF and other factors signaling via JAK/STAT such as angiotensin may act in a compensatory manner to activate the JAK/STAT pathway, thereby maintaining STAT3 phosphorylation, which is crucial for the cellular effects of IL-6 cytokines.
Fuchs et al. (Mon,) conducted a other in Myocardial infarction. IL-6 knockout vs. Wild-type controls was evaluated on MI size, left ventricular remodeling, and mortality. Lack of IL-6 in knockout mice did not affect long-term mortality, myocardial infarction size, or left ventricular remodeling compared to wild-type controls at 6 weeks post-infarction.
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