Excessively chronic inflammation and cardiac fibrosis post myocardial infarction (MI) cause progressive ventricular remodeling, which finally leads to heart failure. We previously found high levels of IL-27 in the heart and serum till day 14 in murine cardiac ischemia-reperfusion injury models. However, whether IL-27 is involved in chronic inflammation-mediated ventricular remodeling remains unclear. In the present study, we found IL-27 levels in serum and damaged heart tissue were elevated and continued to day14 in mice after myocardial infarction. MI triggered high IL-27 expression in cardiac macrophages. The increased expression of IL-27 in the serum is correlated with cardiac dysfunction and fibrosis after MI. Furthermore, addition of IL-27 significantly activated the JAK/STAT signaling pathway in cardiac fibroblasts (CFs). Meanwhile, treatment with IL-27 promoted the proliferation and migration, as well as the differentiation of CFs to myofibroblasts and ECM production induced by angiotensin II (Ang II). Collectively, high level of IL-27 mainly produced by cardiac macrophages post MI promotes the collagen production of CFs and aggravates cardiac fibrosis.
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- EK227
- ELISA试剂盒
Mouse IL-27 ELISA Kit检测试剂盒（酶联免疫吸附法）
- ¥1,600.00 – ¥2,650.00
