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
| Autor: | Han Sun, Changjun Tian, Lin Zhang, Zhihui Zhang, shuhua wu, Cong Ke |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Cell Survival
Inflammation Apoptosis Smad2 Protein 030204 cardiovascular system & hematology Kidney Transforming Growth Factor beta1 03 medical and health sciences 0302 clinical medicine Transforming Growth Factor beta3 Lab/In Vitro Research medicine Gene silencing Humans Viability assay Smad3 Protein Renal Insufficiency Chronic Cell Proliferation Gene knockdown Chemistry Tumor Necrosis Factor-alpha General Medicine Fibrosis Cell biology Cell Aging 030220 oncology & carcinogenesis Tumor necrosis factor alpha RNA Long Noncoding medicine.symptom Signal transduction Transforming growth factor Signal Transduction |
| Zdroj: | Medical Science Monitor : International Medical Journal of Experimental and Clinical Research |
| ISSN: | 1643-3750 1234-1010 |
| Popis: | BACKGROUND Renal fibrosis occurs in the end-stage of all chronic kidney disease. Transforming growth factor-s1 (TGF-s1) is a central contributor in fibrosis. Identifying effective biomarkers that targets TGF-s1 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-s1 induced human kidney 2 (HK-2) cells. MATERIAL AND METHODS We investigated the effects of either overexpression or knockdown of LncRNA-ATB on inflammation, cell apoptosis, and senescence in TGF-s1 induced HK-2 cells. TGF-s1 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)-1s, and IL-6 were measured by corresponding kits. RESULTS LncRNA-ATB was highly expressed in TGF-s1 induced HK-2 cells. Inflammation, cell apoptosis, and senescence were enhanced by TGF-s1 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 TGFs/SMAD2/3 signaling pathway was activated by TGF-s1 and this effect was further enhanced by LncRNA-ATB overexpression. Silencing LncRNA-ATB inhibited the TGFs/SMAD2/3 signaling pathway in TGF-s1 induced cells. The effects of LncRNA-ATB overexpression aforementioned in TGF-s1 induced cells were abolished by blockage of the TGFs/S0MAD2/3 signaling pathway. CONCLUSIONS LncRNA-ATB overexpression have promoting effects on inflammation, cell apoptosis and senescence in TGF-s1 induced HK-2 cells via activating the TGFs/SMAD2/3 signaling pathway. LncRNA-ATB act as a key downstream mediator via activating the TGFs/SMAD2/3 signaling pathway and silencing LncRNA-ATB might be a new strategy for chronic kidney disease treatment. |
| Databáze: | OpenAIRE |
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