ArticleMedical science monitor : international medical journal of experimental and clinical research2020
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.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- TGF-β/Smad Signaling Pathway in Tubulointerstitial Fibrosis.Frontiers in pharmacology · 2022Pooled it
- LncRNA Gm44981 modulates EZH2-H3K27me3-p21 axis to suppress mesangial cell senescence and kidney aging.Renal failure · 2026Article
- LncRNA-ATB Orchestrates Tumor Growth and Immune Responses Through the Modulation of IGF2BP2 in Non-Small-Cell Lung Cancer.IUBMB life · 2026Article
- Rhein alleviates renal interstitial fibrosis by inhibiting Smad3 phosphorylation in TGF-Chinese herbal medicines · 2025Article
- Role of LncRNA in Pathogenesis, Diagnosis and Treatment of Chronic Kidney Disease.Cell biochemistry and biophysics · 2025Review
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Kidney Aging and Chronic Kidney Disease.International journal of molecular sciences · 2024Review
- Roles of long noncoding RNAs in human inflammatory diseases.Cell death discovery · 2024Review
- TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis.Aging and disease · 2023Review
- LncRNA-Dependent Mechanisms of Transforming Growth Factor-β: From Tissue Fibrosis to Cancer Progression.Non-coding RNA · 2022Review
- Review
- Inflammatory Response-Related Long Non-Coding RNA Signature Predicts the Prognosis of Hepatocellular Carcinoma.Journal of oncology · 2022Article
- LncRNA-ATB participates in the regulation of calcium oxalate crystal-induced renal injury by sponging the miR-200 family.Molecular medicine (Cambridge, Mass.) · 2021Article
- Inflammation-Related Long Non-Coding RNA Signature Predicts the Prognosis of Gastric Carcinoma.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Renal fibrosis occurs in the end-stage of all chronic kidney disease. Transforming growth factor-ß1 (TGF-ß1) is a central contributor in fibrosis. Identifying effective biomarkers that targets TGF-ß1 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-ß1 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-ß1 induced HK-2 cells. TGF-ß1 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)-1ß, and IL-6 were measured by corresponding kits. RESULTS LncRNA-ATB was highly expressed in TGF-ß1 induced HK-2 cells. Inflammation, cell apoptosis, and senescence were enhanced by TGF-ß1 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 TGFß/SMAD2/3 signaling pathway was activated by TGF-ß1 and this effect was further enhanced by LncRNA-ATB overexpression. Silencing LncRNA-ATB inhibited the TGFß/SMAD2/3 signaling pathway in TGF-ß1 induced cells. The effects of LncRNA-ATB overexpression aforementioned in TGF-ß1 induced cells were abolished by blockage of the TGFß/S0MAD2/3 signaling pathway. CONCLUSIONS LncRNA-ATB overexpression have promoting effects on inflammation, cell apoptosis and senescence in TGF-ß1 induced HK-2 cells via activating the TGFß/SMAD2/3 signaling pathway. LncRNA-ATB act as a key downstream mediator via activating the TGFß/SMAD2/3 signaling pathway and silencing LncRNA-ATB might be a new strategy for chronic kidney disease treatment.
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