Tubular cell-specific PDGF-B drives fibrogenic niches in kidney fibrosis [RNA-seq_Aging]

Following a transcriptome-wide gene expression analysis of PDGF-B in murine and human kidney cells, we generated transgenic mouse lines with Pdgfb deletion in major expressing cells. Mice with Pdgfb deletion in kidney tubular epithelial cells showed significantly reduced activation and proliferation of peritubular fibroblasts and fibrosis in three models with tubular injury of different etiologies.

We identified paracrine PDGF signaling as a key molecular mechanism of cellular crosstalk mediating the transition of kidney tubular injury to interstitial fibrosis via induction of profibrotic niches.