Glomerular RNA-seq data of the kidney podocyte-specific Hdac1 and Hdac2 deficient mice

Podocyte histone deacetylases (HDAC) are essential in maintaining a normal glomerular filtration barrier by modulating podocyte quiescence. Podocyte-specific loss Hdac1 and 2 in mice results in severe proteinuria and sustained DNA damage, likely caused by epigenetic alterations and deficient DNA repair, that result in podocyte senescence. Through glomeruli isolation and RNA-seq profiling from the mutant mice, we demonstrated that senescent podocytes develop a senescence-associated secretory phenotype (SASP) that contribute to the loss of podocytes. The role of HDACs in senescence may provide important clues in our understanding of how podocytes are lost following injury. Overall design: The freshly glomeruli samples were isolated from the Control mice and HDAC KO mice at 3 weeks of age for the RNAseq analysis. Each sample contained 2 mice in order to get the sufficient glomeruli samples, and 2 independent experiments were analyzed and summarized.