Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis

To gain insight into the differential signaling pathways triggered in N-RAS-/- versus N-RAS+/+ mice during liver injury and fibrosis, we performed microarray analyses of livers 28 days after CCl4 treatment and BDL surgery, respectively. Our findings suggested that increased cell proliferation and matrix deposition as well as loss of cell homeostasis were characteristic of N-RAS-/- after experimental fibrosis. We used microarrays to detail the global programme of gene expression underlying CCl4 and BDL challenge, CCl4 and BDL induced gene expression in livers of N-RAS-/- and N-RAS+/+ mice was measured at 28 days after challenge. Three livers from each group were analyzed in both CCl4 and BDL experiments.