| First Author | Fuchs M | Year | 2003 |
| Journal | FASEB J | Volume | 17 |
| Issue | 14 | Pages | 2118-20 |
| PubMed ID | 12958147 | Mgi Jnum | J:118479 |
| Mgi Id | MGI:3699662 | Doi | 10.1096/fj.03-0331fje |
| Citation | Fuchs M, et al. (2003) Role of interleukin-6 for LV remodeling and survival after experimental myocardial infarction. FASEB J 17(14):2118-20 |
| abstractText | 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. |
