ArticleMedical science monitor : international medical journal of experimental and clinical research2019
miR-34b Alleviates High Glucose-Induced Inflammation and Apoptosis in Human HK-2 Cells via IL-6R/JAK2/STAT3 Signaling Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- IL-6 and diabetic kidney disease.Frontiers in immunology · 2024Review
- Myokines: Novel therapeutic targets for diabetic nephropathy.Frontiers in endocrinology · 2022Review
- miR-34b-5p promotes renal cell inflammation and apoptosis by inhibiting aquaporin-2 in sepsis-induced acute kidney injury.Renal failure · 2021Observational
- Potential role for EZH2 in promotion of asthma through suppression of miR-34b transcription by inhibition of FOXO3.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- Aberrant Methylation of miR-34b and IL-12B mRNA Promoters Contributes to the Reduced Severity of Ankylosing Spondylitis.Biochemical genetics · 2021Article
- Interference of S100A16 suppresses lipid accumulation and inflammation in high glucose-induced HK-2 cells.International urology and nephrology · 2021Article
- TNF-α Receptor Inhibitor Alleviates Metabolic and Inflammatory Changes in a Rat Model of Ischemic Stroke.Antioxidants (Basel, Switzerland) · 2021Article
- Hyperoside Protects HK-2 Cells Against High Glucose-Induced Apoptosis and InflammationPathology oncology research : POR · 2021Article
- The Role of Non-coding RNAs in Diabetic Nephropathy-Related Oxidative Stress.Frontiers in medicine · 2021Review
- Epigenetics and Inflammation in Diabetic Nephropathy.Frontiers in physiology · 2021Review
- Modulation of the Wound Healing through Noncoding RNA Interplay and GSK-3International journal of genomics · 2021Review
- Antimicrobial and Immunomodulatory Activity of Herb Extracts Used in Burn Wound Healing: "San Huang Powder".Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Interference of Hsa_circ_0003928 Alleviates High Glucose-Induced Cell Apoptosis and Inflammation in HK-2 Cells via miR-151-3p/Anxa2.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Non-Coding RNAs as Biomarkers and Therapeutic Targets for Diabetic Kidney Disease.Frontiers in pharmacology · 2020Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND It is well established that inflammation and apoptosis of renal tubular epithelial cells caused by hyperglycemia contribute to the development of diabetic nephropathy (DN). Although microRNAs (miRNAs) are known to have roles in inflammation-related disorders, the exact role of miR-34b in DN has not been defined, and the regulatory mechanism has been unclear. This study aimed to clarify the role of miR-34b in DN pathogenesis. MATERIAL AND METHODS Expression of miR-34b, IL-6R, and other key factors of inflammation, apoptosis (TNF-alpha, IL-1ß, IL-6, caspase-3) in high glucose (HG)-induced HK-2 cells were measured by real-time PCR, Western blot, and flow cytometric cell apoptosis assays. We used luciferase reporter assay to detect the target of miR-34b. Moreover, the targeting gene of miR-34b and its downstream JAK2/STAT3 signaling pathway were explored. RESULTS It was demonstrated that miR-34b overexpression inhibited apoptosis and expression levels of TNF-alpha, IL-1ß, IL-6, and caspase-3 in HG-treated HK-2 cells. We also found that IL-6R is a direct target of miR-34b, which could rescue inflammation and apoptosis in HG-treated HK-2 cells transfected with miR-34b mimic. Furthermore, we showed that overexpression of miR-34b inhibited the IL-6R/JAK2/STAT3 signaling pathway in HG-treated HK-2 cells. CONCLUSIONS Our data suggest that overexpression of miR-34b improves inflammation and ameliorates apoptosis in HG-induced HK-2 cells via the IL-6R/JAK2/STAT3 pathway, indicating that miR-34b could be a promising therapeutic target in DN.
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