Physiological and pathological role of gp130, a common signal transducer for IL-6-family of cytokines

摘要: Receptor complexes for interleukin-6 (IL-6), IL-11, leukemia inhibitory factor (LIF), oncostatin M (OM), ciliary neurotrophic (CNTF) and cardiotrophin-1 (CT-1) utilize membrane glycoprotein gp130 as a common signal-transducing component. In order to investigate detailed physiological roles of determine pathological consequences complete lack or abnormal activation gp130, mice deficient protein expressing continuously activated have been made. A null mutation is lethal, embryos progressively die between 12.5 days post coitum (dpc) term. They show, at 16.5 dpc, hypoplastic development the ventricular myocardium. greatly reduced numbers pluripotential committed hematopoietic progenitors in liver, measured on 13.5 dpc. gp130- / - placentas after 14.5 dpc are smaller than controls exhibit impaired maternofetal transport. Continuous vivo by overexpressing both IL-6 IL-6R leads hypertrophy myocardium thickened walls heart adulthood. These results indicate crucial gp 130 cardiomyocyte regulation, hematopoiesis, placental development.