Long Non-Coding RNA (LncRNA)-ATB Promotes Inflammation, Cell Apoptosis and Senescence in Transforming Growth Factor-β1 (TGF-β1) Induced Human Kidney 2 (HK-2) Cells via TGFβ/SMAD2/3 Signaling Pathway

Background: Renal fibrosis occurs in the end-stage of all chronic kidney disease. Transforming growth factor-beta 1 (TGF-beta 1) is a central contributor in fibrosis. Identifying effective biomarkers that targets TGF-beta 1 is necessary for the development of therapeutic agents for kidney disease. In this study, we investigated the effects and mechanism of long non-coding RNA (LncRNA)-ATB in TGF-beta 1 induced human kidney 2 (HK-2) cells. Material/Methods: We investigated the effects of either overexpression or knockdown of LncRNA-ATB on inflammation, cell apoptosis, and senescence in TGF-beta 1 induced HK-2 cells. TGF-beta 1 induced HK-2 cells served as the cell model. The gene level was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and protein expressions by western blot. Cell Counting Kit-8 (CCK-8) assay was performed for assessment of cell viability. Flow cytometry was applied for detection of cell apoptosis. Tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6 were measured by corresponding kits. Results: LncRNA-ATB was highly expressed in TGF-beta 1 induced HK-2 cells. Inflammation, cell apoptosis, and senescence were enhanced by TGF-beta 1 and these effects were all reduced by knockdown of LncRNA-ATB. Whereas overexpression of LncRNA-ATB had the opposite effects with knockdown of LncRNA-ATB. The TGF beta/SMAD2/3 signaling pathway was activated by TGF-beta 1 and this effect was further enhanced by LncRNA-ATB overexpression. Silencing LncRNA-ATB inhibited the TGFb/SMAD2/3 signaling pathway in TGF-beta 1 induced cells. The effects of LncRNA-ATB overexpression aforementioned in TGF-beta 1 induced cells were abolished by blockage of the TGF beta/S0MAD2/3 signaling pathway. Conclusions: LncRNA-ATB overexpression have promoting effects on inflammation, cell apoptosis and senescence in TGF-beta 1 induced HK-2 cells via activating the TGF beta/SMAD2/3 signaling pathway. LncRNA-ATB act as a key downstream mediator via activating the TGF beta/SMAD2/3 signaling pathway and silencing LncRNA-ATB might be a new strategy for chronic kidney disease treatment.