Y-box-binding protein (YB-1) in murine models of hepatic and renal fibrosis

Background: The Y-box binding protein-1 (YB-1) exerts pleiotropic functions in gene transcription and in translation, e.g. of fibrosis-related genes. Recent in vitro findings point to opposite regulatory effects on fibrogenesis by YB-1 that depend on its subcellular localization. YB-1 might even accomplish opposite functions on gene transcription and mRNA translation of the same gene product, e.g. that of type I collagen (Col1A), a major constituent of the extracellular matrix (ECM) [1]. This led us to in vivo investigations that analyze the outcome of half-maximal YB-1 depletion in a model of liver fibrosis (bile duct ligation (BDL)) and compared the results to renal fibrosis, investigated by unilateral ureteral obstruction (UUO). Additionally, the impact of BDL on kidney damage was assessed.