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RNA-seq transcriptome profiling of HK-2 human renal tubular epithelial cells upon gene knockdown mediated by sgRNA

ABSTRACT: Renal tubular epithelial injury plays a critical role in the progression of renal interstitial fibrosis. In this study, bulk RNA-seq was performed to investigate transcriptomic alterations in human HK-2 proximal tubular epithelial cells following target gene knockdown via sgRNA. Cells transfected with non-targeting sgRNA were used as negative control. Three biological replicates were included for each group. This dataset provides transcriptome resources to uncover molecular events regulated by the target gene in renal tubular epithelial cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE339245 | GEO | 2026/07/25

REPOSITORIES: GEO

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	GSE339245_counts_anno.xls.gz	Xls

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Project description:Renal interstitial fibrosis (RIF) is a common pathological feature and final manifestation of chronic progressive kidney disease. Although exosome-mediated intercellular communication is known to play a crucial role in RIF, the mechanism by which injured tubular epithelial cells (TECs) contribute to fibrogenesis remains incompletely understood. In this study, we investigated the role of exosomal miR-122-5p derived from TECs in modulating fibroblast activation and renal fibrosis. Exosomes were isolated from kidneys of unilateral ureteral obstruction (UUO) mice and from TGF-β1-stimulated HK-2 cells. These exosomes were either co-cultured with fibroblasts (NRK-49F cells) or injected into UUO mice via the tail vein. High-throughput miRNA profiling was used to identify differentially expressed miRNAs in exosomes derived from HK-2 cells, and miR-122-5p was selected for further investigation based on expression level and bioinformatic prediction. Functional analyses were performed using miRNA mimics, inhibitors, and target validation assays. The results showed that exosomal miR-122-5p was significantly downregulated in both fibrotic kidneys and TGF-β1-induced HK-2 cells. In vivo and in vitro, restoration of miR-122-5p levels markedly attenuated renal fibrosis, as evidenced by the reduction of fibrotic markers including α-smooth muscle actin, fibronectin, and collagen I. Mechanistically, miR-122-5p was found to directly target hypoxia-inducible factor 1-alpha (HIF-1α), thereby inhibiting activation of the TGF-β1/Smad signaling pathway. These findings suggest that decreased expression of miR-122-5p in TEC-derived exosomes promotes renal fibrosis through the HIF-1α/TGF-β1/Smad axis, while reintroduction of miR-122-5p can effectively reverse these effects. Taken together, our study provides new insights into the intercellular communication between TECs and fibroblasts via exosomal miRNAs, and identifies miR-122-5p as a potential therapeutic target for the treatment of renal interstitial fibrosis.

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RNA-seq transcriptome profiling of HK-2 human renal tubular epithelial cells upon gene knockdown mediated by sgRNA

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