ArticleInternational journal of molecular medicine2019
miRNA-302e attenuates inflammation in infantile pneumonia though the RelA/BRD4/NF-κB signaling pathway.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- MicroRNA Profiles in Critically Ill Patients.Current medicinal chemistry · 2024Review
- Sphingosine Kinase-1 (SPHK1) promotes inflammation in infantile pneumonia by regulating NLRP3 inflammasome and SIRT1 expression.Histology and histopathology · 2022Article
- The silencing of SAAL1 suppresses pneumonia progression via modulating the NLR signaling pathway.Annals of translational medicine · 2022Article
- Upregulated expression of long non-coding RNA MEG3 serves as a prognostic biomarker in severe pneumonia children and its regulatory mechanism.Bioengineered · 2021Article
- The BET family in immunity and disease.Signal transduction and targeted therapy · 2021Review
- Pharmacological Modulation of BET Family in Sepsis.Frontiers in pharmacology · 2021Review
- JQ1 as a BRD4 Inhibitor Blocks Inflammatory Pyroptosis-Related Acute Colon Injury Induced by LPS.Frontiers in immunology · 2021Article
- Hepatic BRD4 Is Upregulated in Liver Fibrosis of Various Etiologies and Positively Correlated to Fibrotic Severity.Frontiers in medicine · 2021Article
- MicroRNA-127-5p attenuates severe pneumonia via tumor necrosis factor receptor-associated factor 1.Experimental and therapeutic medicine · 2020Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, the main focus was investigating the role of microRNA (miRNA)‑302e in infantile pneumonia (IP) and exploring the potential protective mechanisms. Briefly, the expression of miRNA‑302e was reduced in a mouse model of IP. In addition, the administration of anti‑miRNA‑302e increased inflammation and induced the protein expression of RelA, bromodomain‑containing protein 4 (BRD4) and nuclear factor (NF)‑κB in the in vitro model of IP. In contrast, over‑expression of miRNA‑302e reduced inflammation and suppressed the protein expression of RelA, BRD4 and NF‑κB in an in vitro model of IP. Small interfering (si)‑RelA attenuated the effects of miRNA‑302e on inflammation in an in vitro model of IP. Consistently, si‑BRD4 or si‑NF‑κB attenuated the effects of miRNA‑302e on inflammation in an in vitro model of IP. Taken together, the results of the present study demonstrated that miRNA‑302e attenuated inflammation in IP through the RelA/ BRD4/ NF‑κB signaling pathway.
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