Renal tubular epithelial cells release mediators affecting resident adjacent cells and recruited immune cells, which skews the micromilieu. If perpetuated, these processes lead to maladaptive responses involving loss of tubular cell polarization, cell death, and loss of pericytes or endothelial cells (EndC). The resulting renal fibrosis and vascular rarefication will ultimately impair tubular barrier function. Endogenous tubular cell Regeneration is insufficient for renal repair following chronic stimuli. Especially the intimate crosstalk between tubular cells, EndoC, and infiltrating immune cells and the consequences of these interactions for cell fate decisions remain unknown. Our preliminary data demonstrate that cold shock proteins (e.g. Y-box binding protein-1 (YB-1) and DNA binding protein-A (DbpA)) control monocytic cell recruitment to activated tubular cells and have prominent effects on tubular cell phenotypes and survival. The focus of this Project will be to identify the mechanisms through which cold shock proteins regulate the tubular cell phenotype, the crosstalk with adjacent resident/infiltrating immune cells, and the function of the tubular barrier in chronic renal dysfunction.
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