ArticleMediators of inflammation2016
NF-κB-Regulated miR-99a Modulates Endothelial Cell Inflammation.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- Differential Expression of Small Non-Coding RNAs in Uterine Leiomyomas.International journal of molecular sciences · 2025Article
- Sodium pump subunit NKAα1 protects against diabetic endothelial dysfunction by inhibiting ferroptosis through the autophagy-lysosome degradation of ACSL4.Clinical and translational medicine · 2025Article
- Review
- IL-1β Induces Human Endothelial Surface Expression of IL-15 by Relieving let-7c-3p Suppression of Protein Translation.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- MiR-99a-5p up-regulates LDLR and functionally enhances LDL-C uptake via suppressing PCSK9 expression in human hepatocytes.Frontiers in genetics · 2024Article
- MiR-99a alleviates apoptosis and extracellular matrix degradation in experimentally induced spine osteoarthritis by targeting FZD8.BMC musculoskeletal disorders · 2022Article
- MiRNA-99a alleviates inflammation and oxidative stress in lipopolysaccharide-stimulated PC-12 cells and rats post spinal cord injury.Bioengineered · 2022Article
- Cerebrovascular microRNA Expression Profile During Early Development of Alzheimer's Disease in a Mouse Model.Journal of Alzheimer's disease : JAD · 2022Article
- Exploration of the Molecular Mechanisms ofBioMed research international · 2022Article
- miR-99a regulates CD4Molecular therapy. Nucleic acids · 2021Article
- Inhibition of miR-99a-5p prevents allergen-driven airway exacerbations without compromising type-2 memory responses in the intestine following helminth infection.Mucosal immunology · 2021Article
- The Mechanisms of the Development of Atherosclerosis in Prediabetes.International journal of molecular sciences · 2021Review
- Transcription factor NF-κB promotes acute lung injuryThe Journal of biological chemistry · 2020Article
- The temporal effects of topical NF-Oncotarget · 2020Article
- MicroRNA‑17 contributes to the suppression of the inflammatory response in lipopolysaccharide‑induced acute lung injury in mice via targeting the toll‑like receptor 4/nuclear factor‑κB pathway.International journal of molecular medicine · 2020Article
- Diagnostic, Prognostic, and Therapeutic Value of Non-Coding RNA Expression Profiles in Renal Transplantation.Diagnostics (Basel, Switzerland) · 2020Review
- Inflammation related miRNAs as an important player between obesity and cancers.Journal of diabetes and metabolic disorders · 2019Review
- PCV2 Regulates Cellular Inflammatory Responses through Dysregulating Cellular miRNA-mRNA Networks.Viruses · 2019Article
- MicroRNA-21 inhibits lipopolysaccharide-induced acute lung injury by targeting nuclear factor-κB.Experimental and therapeutic medicine · 2018Article
- Role of Different Blood Purification Nursing Models in Uremic Patients: A Preliminary Report.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective. The present study was performed to investigate the effects and mechanisms of miR-99a on LPS-induced endothelial cell inflammation, as well as the regulation of NF-κB on miR-99a production. Methods and Results. ELISA showed that LPS treatment significantly promoted the secretion of inflammatory factors (TNF-α, IL-6, IL-1β, and MCP-1). LPS treatment also inhibited miR-99a production and promoted mTOR expression and NF-κB nuclear translocation. Overexpression of miR-99a suppressed the LPS-induced TNF-α, IL-6, IL-1β, and MCP-1 overproduction, mTOR upregulation, and NF-κB nuclear translocation. The PROMO software analysis indicated NF-κB binding site in the -1643 to -1652 region of miR-99a promoter. Dual luciferase reporter analysis, electrophoretic mobility shift assays (EMSA), and chromosome immunoprecipitation (ChIP) assays demonstrated that NF-κB promoted the transcription of miR-99a by binding to the -1643 to -1652 region of miR-99a promoter. Further studies on HUVECs verified the regulatory effects of NF-κB on miR-99a production. Conclusion. MiR-99a inhibited the LPS-induced HUVECs inflammation via inhibition of the mTOR/NF-κB signal. NF-κB promoted miR-99a production by binding to the -1643 to -1652 region of miR-99a promoter. Considering the importance of endothelial inflammation on cardiovascular diseases, such as atherosclerosis, our results may provide a new insight into the pathogenesis and therapy of atherosclerosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.