Autor: |
Piobbico D; a Department of Experimental Medicine , University of Perugia , Perugia , Italy., Bartoli D; a Department of Experimental Medicine , University of Perugia , Perugia , Italy., Pieroni S; a Department of Experimental Medicine , University of Perugia , Perugia , Italy., De Luca A; a Department of Experimental Medicine , University of Perugia , Perugia , Italy., Castelli M; a Department of Experimental Medicine , University of Perugia , Perugia , Italy., Romani L; a Department of Experimental Medicine , University of Perugia , Perugia , Italy., Servillo G; a Department of Experimental Medicine , University of Perugia , Perugia , Italy., Della-Fazia MA; a Department of Experimental Medicine , University of Perugia , Perugia , Italy. |
Abstrakt: |
A tight link has been established between inflammation and cancer. Liver regeneration is a widely used model to study the correlation between inflammation and proliferation. IL-6 is essentially involved in liver regeneration and in cancer. Recently, IL-17A has been shown to regulate not only inflammation, but also cell proliferation. Here, we analyze the role played by IL-17A signaling in liver regeneration by comparing cell proliferation in Wild Type and IL-17RA -/- mice. Partial hepatectomy experiments performed in IL-17RA -/- mice showed a delay in expression of early-genes to prime the residual hepatocyte to proliferate, with subsequent delay in G 1 /S-phase transition. We demonstrated that IL-17RA regulates, by recruitment of non-parenchymal cell, the expression of IL-6, which in turn triggers the proliferation of residual hepatocytes. Our data indicate an important role played by IL-17RA in liver proliferation via IL-6. |