Descrição
The glycoprotein 130 (gp130) dependent family of cytokines comprises interleukin-6
(IL-6), IL-11, leukemia inhibitory factor (LIF), cardiotrophin-like cytokine (CLC), ciliary
neurotrophic factor (CNTF), cardiotrophin-1 (CT-1), and oncostatin M (OSM). These
cytokines share the membrane gp130 as a common signal transducer. Recently, it was
demonstrated that IL-6 promotes, whereas LIF inhibits fetal lung branching. Thus, in
this study, the effects on fetal lung morphogenesis of the other classical members of
the gp130-type cytokines (IL-11, CLC, CNTF, CT-1 and OSM) were investigated. We
also provide the first description of these cytokines and their common gp130 receptor
protein expression patterns during rat lung development. Fetal rat lung explants were
cultured in vitro with increasing concentrations of IL-11, CLC, CNTF, CT-1 and OSM.
Treated lung explants were morphometrically analyzed and assessed for MAPK,
PI3K/AKT and STAT3 signaling modifications. IL-11, which similarly to IL-6 acts
through a gp130 homodimer receptor, significantly stimulated lung growth via p38
phosphorylation. On the other hand, CLC, CNTF, CT-1 and OSM, whose receptors are
gp130 heterodimers, inhibited lung growth acting in different signal-transducing
pathways. Thus, the present study demonstrated that although cytokines of the gp130
family share a common signal transducer, there are specific biological activities for
each cytokine on lung development. Indeed, cytokine signaling through gp130
homodimers stimulate, whereas cytokine signaling through gp130 heterodimers inhibit
lung branching.
; Piairo, Paulina C. 
