RNA-sequencing analysis of differential expressed genes in TGFß-treated HK-2 cells after HDAC11 inhibition

Renal fibrosis is a pathological damage associated with nearly all forms of kidney disease. Although a recent study has reported an association between upregulation of histone deacetylase 11 (HDAC11) levels in the kidneys and renal fibrosis in several different mouse models, however, the mechanisms remain elusive. Renal fibrosis is characterized by excessive accumulation of extracellular matrix (ECM), which includes type I and IV collagens, fibronectin and a-smooth muscle actin (a-SMA). The tubular epithelial injury and activation of pro-inflammation contribute to excessive collagen deposition in the pathogenesis of renal fibrosis. Here we aim to explore the role and the underlying mechanisms of HDAC11 in the of progression renal fibrosis. we performed RNA transcriptome sequencing to identify the differentially expressed genes (DEGs) between before and after HDAC11 inhibitor (FT895)-intreated HK-2 cells. GSEA analysis showed that the DEGs were highly enriched in the pathways of epithelial mesenchymal transition and inflammatory response, indicating that HDAC11 inhibitor may resistant to TGFß-induced ECM deposition. Overall design: To investigate the underlying mechanisms of HDAC11 functions in renal fibrosis, we established TGF-beta treated human renal epitehlial cell line HK-2 cells to mimic renal fibrosis.We performed gene expression profiling analysis using RNA-seq data from HK-2 cells treated with TGFb in the absence or presence of HDAC11 selective inhibitor, FT895.Comparative gene expression profiling analysis of RNA-seq data for HK-2 cells treated by TGFb with the presence of DMSO as vehicle (Vehicle+TGFb) and TGFb with the presence of FT895 (FT895+TGFb) for 1h or 12 h.